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Polymorphonuclear Leukocytes (polymorphonuclear + leukocyte)
Kinds of Polymorphonuclear Leukocytes Selected AbstractsEffect Of E. faecalis On The Release Of Serine Proteases Elastase And Cathepsin G, And Collagenase-2 (MMP-8) By Human Polymorphonuclear Leukocytes (PMNs)AUSTRALIAN ENDODONTIC JOURNAL, Issue 3 2005Article first published online: 11 FEB 2010 No abstract is available for this article. [source] Areca nut extracts-activated secretion of leukotriene B4, and phosphorylation of p38 mitogen-activated protein kinase and elevated intracellular calcium concentrations in human polymorphonuclear leukocytesJOURNAL OF PERIODONTAL RESEARCH, Issue 5 2007S.-L. Hung Background and Objective:, Polymorphonuclear leukocytes are the major source of leukotriene B4, which is synthesized via the 5-lipoxygenase pathway. Activation of the 5-lipoxygenase pathway is regulated by intracellular calcium and the phosphorylation of p38 mitogen-activated protein kinase (MAPK). The impact of areca nut extracts on the biosynthesis of leukotriene B4 by human polymorphonuclear leukocytes was evaluated, and some of the possible mechanisms underlying the responses were examined. Material and Methods:, Polymorphonuclear leukocytes were treated with various concentrations of areca nut extracts. The concentrations of leukotriene B4 released into the supernatants were evaluated using enzyme immunoassay. The phosphorylation of p38 MAPK was monitored using immunoblotting, and the cytosolic calcium kinetics were assessed fluorometrically using Fura-2. Results:, Exposure of polymorphonuclear leukocytes to areca nut extracts led to a dose-dependent increase in the production of leukotriene B4, with levels peaking at 30 min and decreasing thereafter. Areca nut extracts enhanced the phosphorylation of p38 MAPK, an enzyme known to activate 5-lipoxygenase. Incubation with areca nut extracts also resulted in a rapid elevation of intracellular calcium concentrations in polymorphonuclear leukocytes. The induction of leukotriene B4 by areca nut extracts was suppressed with the p38 MAPK inhibitor, SB203580, or with the intracellular calcium chelator, BAPTA-AM. Conclusion:, The interaction of areca nut extracts with polymorphonuclear leukocytes activated the arachidonic acid metabolic cascade. Incubation of polymorphonuclear leukocytes with areca nut extracts resulted in the activation of intracellular events, such as phosphorylation of p38 MAPK and Ca2+ mobilization, involved in the release of pro-inflammatory lipid mediators. The results of this study emphasize the potential importance of polymorphonuclear leukocytes as a source of leukotriene B4, which may modulate the inflammatory response in areca chewers. [source] Smoke Exposure and Ethanol Ingestion Modulate Intrapulmonary Polymorphonuclear Leukocyte Killing, but Not Recruitment or PhagocytosisALCOHOLISM, Issue 9 2006Elizabeth A. Vander Top Background: People who smoke and abuse alcohol are uniquely susceptible to pulmonary infections caused by Streptococcus pneumoniae, the pneumococcus. The primary cellular defense against pneumococci within the lungs is the polymorphonuclear leukocyte (PMN). Cigarette smoke and ethanol (EtOH) are known to alter certain PMN functions, but little is known about their concurrent effects. Methods: Male Sprague,Dawley rats were exposed twice daily for 8 weeks to cigarette smoke (smoke-exposed) or room air (sham-exposed). During the final week of exposure, the rats were pair-fed a liquid diet containing either 36 or 0% EtOH calories. Polymorphonuclear leukocytes were prerecruited into the rats' lungs by transtracheal injection of lipopolysaccharide. Five hours later, the rats were infected transtracheally with S. pneumoniae, and PMN recruitment, phagocytosis, and bactericidal activity were quantified within their lungs. Chemokine levels were also measured in bronchoalveolar lavage fluids, lung homogenates, and sera. Results: Neither PMN recruitment nor phagocytic uptake of pneumococci was altered by EtOH ingestion or smoke exposure. Killing of the organisms, however, was significantly decreased in sham-exposed, but not smoke-exposed, rats ingesting EtOH. Parallel results were determined for serum cytokine-induced neutrophil chemoattractant-1 (CINC-1), with EtOH ingestion significantly decreasing the levels in sham-exposed, but not smoke-exposed, rats. Pulmonary levels of macrophage inflammatory protein-2 (MIP-2) and CINC-1 were highly elevated by the combination of EtOH and smoke. Conclusions: One week of EtOH ingestion by rats impaired the ability of their PMNs to kill S. pneumoniae within their lungs. This was not due to decreased recruitment of the PMNs to the lungs or to diminished phagocytosis of intrapulmonary pneumococci. The addition of twice-daily cigarette smoke exposure to this short-term EtOH ingestion model restored PMN bactericidal ability to levels observed in the absence of either treatment. These EtOH-induced and smoke-induced alterations in PMN killing may be related to alterations in both pulmonary and systemic inflammatory chemokine levels. [source] Significant differences between capillary and venous complete blood counts in the neonatal periodINTERNATIONAL JOURNAL OF LABORATORY HEMATOLOGY, Issue 1 2003S.M. Kayiran Summary The normal capillary and venous hematologic values for neonates have not been defined clearly. It is well known that capillary blood has higher hemoglobin (Hb) and hematocrit (Hct) values than venous blood. In a recent study, we reported differences between capillary and venous complete blood counts (CBC) in healthy term neonates on day 1 of life. The aim of this study was to extend our previous investigation. Term neonates (n=141) were stratified into four groups by days of postnatal age: group 2 (day 7, n=38), group 3 (day 14, n=35), group 4 (day 21, n=32) and, group 5 (day 28, n=36). Data from our previous study were included in the statistical analysis as group 1 (day 1, n=95). A CBC and differential count were carried out on each capillary and venous sample drawn simultaneously. Within each group, the mean and standard deviation for each parameter in capillary and venous blood were calculated and then compared using the paired sample t -test. In all groups, the capillary blood samples had higher Hb, Hct, red blood cell (RBC), white blood cell (WBC), and lymphocyte counts. In each group, venous platelet counts were significantly higher than the corresponding capillary values. There was also a trend toward higher venous mean corpuscular volume, higher capillary polymorphonuclear leukocyte (PML) count and mean platelet volume in all groups. In both capillary and venous blood, Hb, Hct, RBC, MCV values and WBC, lymphocyte, PML counts decreased and platelet counts increased steadily during neonatal period. This study reveals that CBC parameters and differential counts may differ depending on the blood sampling used. The findings underline the importance of considering the sample source when using hematologic reference ranges for healthy or septic neonates. When interpreting results, the term ,peripheral blood' should be replaced with ,capillary blood' or ,venous blood' so that an accurate assessment can be made. [source] Sister chromatid exchange and micronucleus studies in patients with Behçet's diseaseJOURNAL OF CUTANEOUS PATHOLOGY, Issue 8 2009Ali Karaman Background:, Genetic factors that predispose individuals to Behçet's disease (BD) are considered to play important roles in the development of the disease. The aim of this study was to determine, by counting sister chromatid exchange (SCE) and micronucleus (MN) frequencies, whether DNA damage have an effect on the pathogenesis of BD. Furthermore, our aim was to show if there is an association between oxidative stress and chromosome instability in BD. Methods:, We analyzed lymphocytes from patients with BD (16 in active and 14 in inactive periods) and 20 healthy controls for SCE and MN frequencies. In addition, malondialdehyde (MDA) level, superoxide dismutase (SOD) level, glutathione peroxidase (GSH-Px) activity, erythrocyte sedimentation rate (ESR) and polymorphonuclear leukocyte (PMNL) count were determined in the all subjects. Results:, The SCE and MN frequencies were significantly higher in both the active and inactive period patients than in the controls (p < 0.00001, p < 0.0001, p < 0.01 and p < 0.05, respectively), and the MDA level was significantly higher in both the active and inactive period patients than in the controls (p < 0.01 and p < 0.05, respectively). In contrast, the SOD and GSH-Px levels were significantly lower in both the active and inactive period patients than in the controls (p < 0.01, p < 0.05, p < 0.01 and p < 0.05, respectively). Conclusions:, Our results suggest that increased plasma MDA level and decreased plasma GSH-Px and SOD levels reflect the increased levels of oxidative stress in BD patients, and this situation may impair genetic stability in BD patients. [source] Smoke Exposure and Ethanol Ingestion Modulate Intrapulmonary Polymorphonuclear Leukocyte Killing, but Not Recruitment or PhagocytosisALCOHOLISM, Issue 9 2006Elizabeth A. Vander Top Background: People who smoke and abuse alcohol are uniquely susceptible to pulmonary infections caused by Streptococcus pneumoniae, the pneumococcus. The primary cellular defense against pneumococci within the lungs is the polymorphonuclear leukocyte (PMN). Cigarette smoke and ethanol (EtOH) are known to alter certain PMN functions, but little is known about their concurrent effects. Methods: Male Sprague,Dawley rats were exposed twice daily for 8 weeks to cigarette smoke (smoke-exposed) or room air (sham-exposed). During the final week of exposure, the rats were pair-fed a liquid diet containing either 36 or 0% EtOH calories. Polymorphonuclear leukocytes were prerecruited into the rats' lungs by transtracheal injection of lipopolysaccharide. Five hours later, the rats were infected transtracheally with S. pneumoniae, and PMN recruitment, phagocytosis, and bactericidal activity were quantified within their lungs. Chemokine levels were also measured in bronchoalveolar lavage fluids, lung homogenates, and sera. Results: Neither PMN recruitment nor phagocytic uptake of pneumococci was altered by EtOH ingestion or smoke exposure. Killing of the organisms, however, was significantly decreased in sham-exposed, but not smoke-exposed, rats ingesting EtOH. Parallel results were determined for serum cytokine-induced neutrophil chemoattractant-1 (CINC-1), with EtOH ingestion significantly decreasing the levels in sham-exposed, but not smoke-exposed, rats. Pulmonary levels of macrophage inflammatory protein-2 (MIP-2) and CINC-1 were highly elevated by the combination of EtOH and smoke. Conclusions: One week of EtOH ingestion by rats impaired the ability of their PMNs to kill S. pneumoniae within their lungs. This was not due to decreased recruitment of the PMNs to the lungs or to diminished phagocytosis of intrapulmonary pneumococci. The addition of twice-daily cigarette smoke exposure to this short-term EtOH ingestion model restored PMN bactericidal ability to levels observed in the absence of either treatment. These EtOH-induced and smoke-induced alterations in PMN killing may be related to alterations in both pulmonary and systemic inflammatory chemokine levels. [source] Cryopreservable neutrophil surrogates: Granule-poor, motile cytoplasts from polymorphonuclear leukocytes home to inflammatory lesions in vivoCYTOSKELETON, Issue 5 2006Stephen E. Malawista Abstract Cytokineplasts (CKP) are anucleate, motile, granule-poor fragments induced from polymorphonuclear leukocytes on surfaces by the brief application of heat. Derived from the peripheral cytoplasm and membranes of PMN, they retain the sensing, transducing, and effector mechanisms necessary for chemotaxis and phagocytosis, and appear to represent a functional, self-purification of the motile apparatus. Unlike their parent PMN, CKP are cryopreservable. We have shown that they can adhere to endothelial cell monolayers, open interendothelial cell junctions, and migrate to the abluminal side when stimulated by a chemoattractant. Employing an animal model, we now show that, given intravenously, they can home to an inflammatory target lesion in vivo. Cell Motil. Cytoskeleton 2006. © 2006 Wiley-Liss, Inc. [source] The chemotaxis defect of Shwachman-Diamond Syndrome leukocytesCYTOSKELETON, Issue 3 2004Vesna Stepanovic Abstract Shwachman-Diamond Syndrome (SDS) is a rare autosomal recessive, multisystem disorder presenting in childhood with intermittent neutropenia and pancreatic insufficiency. It is characterized by recurrent infections independent of neutropenia, suggesting a functional neutrophil defect. While mutations at a single gene locus (SBDS) appear to be responsible for SDS in a majority of patients, the function of that gene and a specific defect in SDS neutrophil behavior have not been elucidated. Therefore, employing 2D and 3D computer-assisted motion analysis systems, we have analyzed the basic motile behavior and chemotactic responsiveness of individual polymorphonuclear leukocytes (PMNs) of 14 clinically diagnosed SDS patients. It is demonstrated that the basic motile behavior of SDS PMNs is normal in the absence of chemoattractant, that SDS PMNs respond normally to increasing and decreasing temporal gradients of the chemoattractant fMLP, and that SDS PMNs exhibit a normal chemokinetic response to a spatial gradient of fMLP. fMLP receptors were also distributed uniformly through the plasma membrane of SDS PMNs as in control PMNs. SDS PMNs, however, were incapable of orienting in and chemotaxing up a spatial gradient of fMLP. This unique defect in orientation was manifested by the PMNs of every SDS patient tested. The PMNs of an SDS patient who had received an allogenic hematopoietic stem cell transplant, as well as PMNs from a cystic fibrosis patient, oriented normally. These results suggest that the defect in SDS PMNs is in a specific pathway emanating from the fMLP receptor that is involved exclusively in regulating orientation in response to a spatial gradient of fMLP. This pathway must function in parallel with additional pathways, intact in SDS patients, that emanate from the fMLP receptor and regulate responses to temporal rather than spatial changes in receptor occupancy. Cell Motil. Cytoskeleton 57:158,174, 2004. © 2004 Wiley-Liss, Inc. [source] Methylene blue attenuates lung injury after mesenteric artery clamping/unclampingEUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 6 2004A. A. Weinbroum Abstract Background, This controlled, experimental study was designed to assess the effects of intratracheal and intravenous methylene blue on reperfusion lung injury following superior mesenteric artery clamping/unclamping. Materials and methods, Superior mesenteric arteries of 144 anaesthetized adult male Wistar rats (n = 12/group) were clamped for 1 h. Ten minutes before unclamping, methylene blue or its vehicle was administered intratracheally or intravenously, followed by a 3 h-respiratory assessment and postexperimental assessment of survival. Results, Intravenous 3 and 9 mg kg,1 but not higher methylene blue doses, and intratracheal 6-mg kg,1 but not lower doses, significantly (P < 0·05) reduced the 100% increase in plateau pressure, 30% reduction in PO2/FiO2, fourfold augmented bronchoalveolar lavage-retrieved volume and the increased polymorphonuclear leukocytes/bronchoalveolar cells' ratio associated with unclamping of the superior mesenteric artery. Lung tissue polymorphonuclear leukocytes count, total xanthine oxidase activity and wet-to-dry-weight ratio were also normal in these dose-treated groups. These effective regimens were also associated with longer animal survival. Conclusions, Intratracheal methylene blue mitigates lung reperfusion injury following superior mesenteric artery clamping/unclamping at a similar magnitude as an intravenous regimen. This finding is a novel potential use of methylene blue in vivo. [source] Oxidative stress in red blood cells, platelets and polymorphonuclear leukocytes from patients with myelodysplastic syndromeEUROPEAN JOURNAL OF HAEMATOLOGY, Issue 6 2007Hussam Ghoti Abstract Low-risk myelodysplastic syndrome (MDS) is characterized by cytopenia, mainly anemia, because of ineffective hematopoiesis. Some of the patients with ineffective erythropoiesis, with or without ring sideroblasts in their bone marrow, develop severe anemia requiring frequent blood transfusions and consequently develop iron overload. Excess free iron in cells catalyses the generation of reactive oxygen species (ROS) that cause cell and tissue damage. Using flow cytometry techniques, we compared the oxidative status of red blood cells (RBC), platelets and neutrophils in 14 MDS patients with those of normal donors. The results show that ROS were higher while reduced glutathione (GSH) was lower in their RBC and platelets compared with normal cells. In neutrophils, no difference was found in ROS, while the GSH levels were lower. A correlation (r = 0.6) was found between serum ferritin levels of the patients and the ROS in their RBC and platelets. The oxidative stress was ameliorated by a short incubation with the iron-chelators, the deferrioxamine and deferiprone or with antioxidants such as N -acetylcysteine, suggesting that MDS patients might benefit from treatment with iron-chelators and antioxidants. [source] The expression of cytosolic phospholipase A2 and biosynthesis of leukotriene B4 in acute myeloid leukemia cellsEUROPEAN JOURNAL OF HAEMATOLOGY, Issue 6 2007Gudmundur Runarsson Abstract Leukotrienes (LT) exert stimulatory effects on myelopoiesis, beside their inflammatory and immunomodulating effects. Here, we have studied the expression and activity of the enzymes involved in the synthesis of leukotriene B4 (LTB4) in acute myeloid leukemia (AML) cells (16 clones) and G-CSF mobilized peripheral blood CD34+ cells. CD34+ cells from patients with non-myeloid malignancies expressed cytosolic phospholipase A2 (cPLA2), 5-lipoxygenase activating protein (FLAP), and leukotriene A4 (LTA4) hydrolase but not 5-lipoxygenase (5-LO). The enzyme cPLA2 was abundantly expressed in AML cells and the activity of the enzyme was high in certain AML clones. The expression of 5-LO, FLAP, and LTA4 hydrolase in AML clones was in general lower than in healthy donor polymorphonuclear leukocytes (PMNL). The calcium ionophore A23187-induced release of [14C] arachidonic acid (AA) in AML cells was low, compared with PMNL, and did not correlate with the expression of cPLA2 protein. Biosynthesis of LTB4, upon calcium ionophore A23187 activation, was only observed in five of the investigated AML clones and only three of the most differentiated clones produced similar amounts of LTB4 as PMNL. The capacity of various cell clones to produce LTs could neither be explained by the difference in [1 , 14C] AA release nor 5-LO expression. Taken together, these results indicate that LT synthesis is under development during early myelopoiesis and the capacity to produce LTs is gained upon maturation. High expression of cPLA2 in AML suggests a putative role of this enzyme in the pathophysiology of this disease. [source] ADAM17 activity during human neutrophil activation and apoptosisEUROPEAN JOURNAL OF IMMUNOLOGY, Issue 4 2006Bruce Walcheck Dr. Abstract Substrates of the metalloprotease ADAM17 (also known as TNF-, converting enzyme or TACE) undergo ectodomain shedding and include various inflammatory modulators. Though polymorphonuclear leukocytes contribute significantly to inflammation, direct analyses of ADAM17 on human neutrophils are very limited. In addition, the current understanding of the processes regulating ADAM17 activity primarily relate to its rapid activation. Therefore, to extend insights into the mechanisms of ADAM17 activity, we examined its surface expression and the shedding of its substrates during extended periods of neutrophil activation and apoptosis. Contrary to studies with immortalized hematopoietic cell lines, we report that surface expression of ADAM17 is maintained by human neutrophils activated with formyl peptides or by FcR/complement receptor-mediated phagocytosis. Interestingly, bacterial phagocytosis resulted in a significant increase in ADAM17 expression several hours after pathogen engulfment. We provide novel evidence that ADAM17 surface expression is also maintained during spontaneous and anti-Fas-induced neutrophil apoptosis. The well-validated ADAM17 substrates L-selectin and proTNF-, were shed efficiently by neutrophils under each of the conditions tested. Our data thus indicate prolonged ADAM17 expression during neutrophil effector functions. The implications of this may be a role by ADAM17 in both the induction and down-regulation of neutrophil activity. [source] Chlamydiae and polymorphonuclear leukocytes: unlikely allies in the spread of chlamydial infectionFEMS IMMUNOLOGY & MEDICAL MICROBIOLOGY, Issue 1 2008Roger G. Rank Abstract While much is known about the attachment of the chlamydiae to the host cell and intracellular events during the developmental cycle, little is known about the mechanism(s) by which elementary bodies exit the cell. In this report, we use the guinea-pig conjunctival model of Chlamydia caviae infection to present in vivo ultrastructural evidence supporting two mechanisms for release of chlamydiae from the mucosal epithelia. Four days after infection, histopathologic observation shows an intense infiltration of polymorphonuclear leukocytes (PMN) in the conjunctival epithelium. Using transmission electron microscopy, a gradient-directed PMN response to chlamydiae-infected epithelial cells was observed. As PMN infiltration intensifies, epithelial hemidesmosome/integrin/focal adhesion adherence with the basal lamina is disconnected and PMNs literally lift off and release infected superficial epithelia from the mucosa. Many of these infected cells appear to be healthy with intact microvilli, nuclei, and mitochondria. While lysis of some infected cells occurs with release of chlamydiae into the extracellular surface milieu, the majority of infected cells are pushed off the epithelium. We propose that PMNs play an active role in detaching infected cells from the epithelium and that these infected cells eventually die releasing organisms but, in the process, move to new tissue sites via fluid dynamics. [source] Proper expression of the O-antigen of lipopolysaccharide is essential for the virulence of Yersinia enterocolitica O:8 in experimental oral infection of rabbitsFEMS IMMUNOLOGY & MEDICAL MICROBIOLOGY, Issue 2 2003H Najdenski Abstract The O-antigen of lipopolysaccharide (LPS) is required for virulence in Yersinia enterocolitica serotype O:8. Here we evaluated the importance of controlling the O-antigen biosynthesis using an in vivo rabbit model of infection. Y. enterocolitica O:8 wild-type strain was compared to three mutants differing in the O-antigen phenotype: (i) the rough strain completely devoid of the O-antigen, (ii) the wzy strain that lacks the O-antigen polymerase (Wzy protein) and expresses LPS with only one repeat unit, and (iii) the wzz strain that lacks the O-antigen chain length determinant (Wzz protein) and expresses LPS without modal distribution of O-antigen chain lengths. The most attenuated strain was the wzz mutant. The wzz bacteria were cleared from the tissues by day 30, the blood parameters were least dramatic and histologically only immunomorphological findings were seen. The level of attenuation of the rough and the wzy strain bacteria was between the wild-type and the wzz strain. Wild-type bacteria were highly resistant to killing by polymorphonuclear leukocytes, the wzz strain bacteria were most sensitive and the rough and wzy strain bacteria were intermediate resistant. These results clearly demonstrated that the presence of O-antigen on the bacterial surface is not alone sufficient for full virulence, but also there is a requirement for its controlled chain length. [source] HIV protease inhibitors attenuate adherence of Candida albicans to epithelial cells in vitroFEMS IMMUNOLOGY & MEDICAL MICROBIOLOGY, Issue 1 2001Jasmin Bekti Abstract Oropharyngeal candidiasis is one of the first and most commonly reported opportunistic infections of untreated AIDS patients. With the introduction of the new antiviral HAART therapy, including HIV protease inhibitors, this mucocutaneous infection is nowadays only rarely observed in treated patients. It was recently shown that HIV protease inhibitors have a direct attenuating effect on Candida albicans secreted aspartic proteinases (Saps), an investigation prompted by the fact that both Sap and HIV protease belong to the superfamily of aspartic proteinases and by the observation that mucocutaneous infections sometimes resolve even in the absence of an immunological improvement of the host. As these Saps are important fungal virulence factors and play a key role in adhesion to human epithelial cells we tried to assess the effect of the HIV protease inhibitors Ritonavir, Indinavir and Saquinavir on fungal adhesion to these cells. The effect on phagocytosis by polymorphonuclear leukocytes was also assessed. Ritonavir was found to be the most potent inhibitor of fungal adhesion. A dose-dependent inhibition of adhesion to epithelial cells was found already at 0.8 ,M and was significant at 4 ,M or higher, at 500 ,M the inhibition was about 55%. Indinavir and Saquinavir inhibited significantly at 4 ,M or 20 ,M, respectively; at 500 ,M the inhibition was 30% or 50%. In contrast, no protease inhibitor was able to modulate phagocytosis of Candida by polymorphonuclear leukocytes. In conclusion, inhibition of Saps by HIV protease inhibitors may directly help to ease the resolution of mucosal candidiasis. In future, derivatives of HIV protease inhibitors, being more specific for the fungal Saps, may form an alternative in the treatment of mucosal candidiasis insensitive to currently available antimycotics. [source] High-dose methylprednisolone influences the physiology and virulence of Candida albicans ambiguously and enhances the candidacidal activity of the polyene antibiotic amphotericin B and the superoxide-generating agent menadioneFEMS YEAST RESEARCH, Issue 2 2007Ágnes Gyetvai Abstract Although exposure of Candida albicans cells to high-dose (4 mM) methylprednisolone stimulated microbial growth, germination rate in serum and phospholipase release, it also promoted the recognition of C. albicans cells by polymorphonuclear leukocytes. Pretreatment of C. albicans cells with methylprednisolone did not result in any increase in the pathogenicity of the fungus in intraperitoneal and intravenous mouse assays. Therefore, the virulence of C. albicans is unlikely to increase in patients treated with comparably high-dose methylprednisolone on skin and mucosal membranes. Methylprednisolone treatments also increased the production of conjugated dienes and thiobarbituric acid-reactive substances, and the menadione sensitivity of C. albicans cells, which can be explained by a significant decrease in the specific activities of several antioxidant enzymes. The combination of methylprednisolone with oxidants, e.g. in topical applications, may be of clinical importance when the predisposition to candidiasis is high. Methylprednisolone treatments negatively affected membrane fluidity and decreased the antifungal effects of both the polyene antibiotic nystatin and the ergosterol biosynthesis inhibitor lovastatin, and also enhanced the deleterious effects of the polyene antimycotic amphotericin B on C. albicans cells. These corticosteroid,polyene drug interactions should be considered in the treatment of C. albicans infections in patients with prolonged topical application of corticosteroids. [source] Less-oxidative hemodialysis solution rendered by cathode-side application of electrolyzed waterHEMODIALYSIS INTERNATIONAL, Issue 3 2007Masaaki NAKAYAMA Abstract Electrolyzed water (EW) generated on the cathode side reportedly displays anti-oxidative properties, and application of EW to hemodialysis (HD) systems supposedly suppresses oxidative markers in patients on HD. However, most of the chemical properties and biological effects of such solutions remain unclear. This study aimed to examine those issues to clarify the scientific background for the clinical use of EW solution. Reverse osmosis water comprising EW from the cathode side (e-RO) was prepared and used to process a test HD solution (e-HD). Chemical and biological properties of these solutions were compared with controls. Redox properties were examined by chemiluminescence (CL) of the luminol-H2O2 system. Biological effects of e-RO on human polymorphonuclear leukocytes (PMNs) were tested with respect to the cellular protection against methylglyoxal, and with respect to the preservation of cellular function as to radical generation. Control HD solution presented the highest CL, followed by e-HD, control RO, suggesting a lower oxidative capacity for EW-based solutions. Increased levels of dissolved hydrogen were characteristic of e-RO and e-HD. Application of e-RO tended to be associated with less injury of PMNs by methylglyoxal, and with significantly higher levels of radical generation compared with the control. Compared with control HD, e-RO-based HD solution displays less-oxidative capacity in chemical terms, and may at least partly facilitate preservation of PMN viability. These results appear to offer a scientific basis for supporting the clinical challenge of applying this technology to HD treatment. [source] Pathophysiologic importance of E- and L-selectin for neutrophil-induced liver injury during endotoxemia in miceHEPATOLOGY, Issue 5 2000Judy A. Lawson Neutrophils can cause parenchymal cell injury in the liver during ischemia-reperfusion and endotoxemia. Neutrophils relevant for the injury accumulate in sinusoids, transmigrate, and adhere to hepatocytes. To investigate the role of E- and L-selectin in this process, C3Heb/FeJ mice were treated with 700 mg/kg galactosamine and 100 ,g/kg endotoxin (Gal/ET). Immunogold labeling verified the expression of E-selectin on sinusoidal endothelial cells 4 hours after Gal/ET injection. In addition, Gal/ET caused up-regulation of Mac-1 (CD11b/CD18) and shedding of L-selectin from circulating neutrophils. Gal/ET induced hepatic neutrophil accumulation (422 ± 32 polymorphonuclear leukocytes [PMN]/50 high power fields [HPF]) and severe liver injury (plasma alanine transaminase [ALT] activities: 4,120 ± 960 U/L; necrosis: 44 ± 3%) at 7 hours. Treatment with an anti,E-selectin antibody (3 mg/kg, intravenously) at the time of Gal/ET administration did not significantly affect hepatic neutrophil accumulation and localization. However, the anti,E-selectin antibody significantly attenuated liver injury as indicated by reduced ALT levels (,84%) and 43% less necrotic hepatocytes. In contrast, animals treated with an anti,L-selectin antibody or L-selectin gene knock out mice were not protected against Gal/ET-induced liver injury. However, E-, L-, and P-selectin triple knock out mice showed significantly reduced liver injury after Gal/ET treatment as indicated by lower ALT levels (,65%) and reduced necrosis (,68%). Previous studies showed that circulating neutrophils of E-selectin,overexpressing mice are primed and activated similar to neutrophils adhering to E-selectin in vitro. Therefore, we conclude that blocking E-selectin or eliminating this gene may have protected against Gal/ET-induced liver injury in vivoby inhibiting the full activation of neutrophils during the transmigration process. [source] Treatment of men with urethritis negative for Neisseria gonorrhoeae, Chlamydia trachomatis, Mycoplasma genitalium, Mycoplasma hominis, Ureaplasma parvum and Ureaplasma urealyticumINTERNATIONAL JOURNAL OF UROLOGY, Issue 5 2007Shin-Ichi Maeda Objective: Some patients with symptomatic non-gonococcal urethritis (NGU) are negative for Chlamydia trachomatis, mycoplasmas and ureaplasmas. The optimal antimicrobial chemotherapy for such NGU has not fully been elucidated, though many studies of antimicrobial chemotherapies for C. trachomatis -positive NGU have been performed. We assessed the efficacy of antimicrobial agents that are active against C. trachomatis on non-mycoplasmal, non-ureaplasmal and non-chlamydial NGU (NMNUNCNGU). Methods: One hundred men whose first-pass urine samples were negative for C. trachomatis, Mycoplasma genitalium, Mycoplasma hominis, Ureaplasma parvum, and Ureaplasma urealyticum were treated with levofloxacin, gatifloxacin, minocycline, or clarithromycin for 7 days. Urethritis symptoms and the presence of polymorphonuclear leukocytes (PMNL) in urethral smears were assessed before and after treatment. Results: Eighty-eight (88.0%) of 100 men with NMNUNCNGU showed no signs of urethral inflammation after treatment, but two men complained of some symptoms of urethritis. Twelve (12.0%) of 100 men had significant numbers of PMNL in urethral smears, but five of these 12 men had no symptoms of urethritis. The efficacy for normalization of urethral smears was 90.7% for clarithromycin, 89.7% for levofloxacin, 87.5% for gatifloxacin, and 75.0% for minocycline. The 12 men who showed signs of urethral inflammation were retreated with levofloxacin, gatifloxacin, minocycline or clarithromycin for an additional 7 days. The 10 men who returned after the second treatment had negative urethral smears. Conclusion: Our present findings suggest that antimicrobial agents active against C. trachomatis are effective against NMNUNCNGU and that a 7-day treatment regimen with an appropriate antimicrobial agent may be sufficient to manage patients with NMNUNCNGU. [source] TT virus (TTV) loads associated with different peripheral blood cell types and evidence for TTV replication in activated mononuclear cellsJOURNAL OF MEDICAL VIROLOGY, Issue 2 2001Fabrizio Maggi Abstract TT virus (TTV) loads associated with the peripheral blood cells of seven patients known to carry the virus in plasma were investigated by real-time PCR. Whereas red cells/platelets were uniformly negative, six and four patients yielded positive peripheral blood mononuclear cells (PBMCs) and polymorphonuclear leukocytes, respectively, but viral titres were generally low. Fractionation of PBMCs into monocyte- and B, T4, and T8 lymphocyte-enriched subpopulations showed no pattern in the viral loads that might suggest the preferential association of TTV to one or more specific cell types. TTV-negative PBMCs absorbed measurable amounts of virus when incubated with infected plasma at 4°C. Furthermore, cultures of TTV-negative phytohaemagglutinin-stimulated PBMCs exposed in vitro to virus-positive plasma and faecal extracts released considerable levels of infectious TTV into the supernatant fluid and the same was true for TTV-positive stimulated PBMCs. These results indicate that, whereas freshly harvested resting PBMCs seem to produce little, if any TTV, stimulated PBMCs actively replicate the virus. J. Med. Virol. 64:190,194, 2001. © 2001 Wiley-Liss, Inc. [source] Areca nut extract-treated gingival fibroblasts modulate the invasiveness of polymorphonuclear leukocytes via the production of MMP-2JOURNAL OF ORAL PATHOLOGY & MEDICINE, Issue 1 2009Hsuan-Hsuan Lu Background:, Areca nut chewing is associated with an increase in the incidence of oral neoplastic or inflammatory diseases. Aberrations in matrix metalloprotease (MMP) expression are associated with the pathogenesis of oral diseases. This study investigated the potential effects of areca nut extract (ANE) on human gingival fibroblasts and the consequential impacts on inflammatory pathogenesis. Methods:, Analyses of senescence marker, cell viability, changes of the cell cycle, and cell granularity in gingival fibroblasts together with an assessment of the invasiveness of polymorphonuclear (PMN) leukocytes after treatment with the supernatant of ANE-treated gingival fibroblasts were performed to characterize the phenotypic impacts. Western blotting and gelatin zymography were used to assay the expression and activity of MMP-2. Results:, Chronic subtoxic (<10 ,g/ml) ANE treatment resulted in premature growth arrest, appearance of senescence-associated ,-galactosidase activity and various other senescence-associated phenotypes in gingival fibroblasts. Gingival fibroblasts established from older individuals had a higher propensity to become ANE-induced senescent gingival fibroblasts. An activation of MMP-2 was identified in senescent cells. PMN leukocytes treated with the supernatant of ANE-induced senescent cells exhibited a significant increase in invasiveness, which was abrogated by both a MMP-2 blocker and a MMP-2 nullifying antibody. Conclusions:, This study provides evidence whereby MMP-2 secreted from ANE-induced senescent gingival fibroblasts would facilitate the invasiveness of PMN leukocytes, which could be associated with the oral inflammatory process in areca chewers. [source] Areca nut extracts-activated secretion of leukotriene B4, and phosphorylation of p38 mitogen-activated protein kinase and elevated intracellular calcium concentrations in human polymorphonuclear leukocytesJOURNAL OF PERIODONTAL RESEARCH, Issue 5 2007S.-L. Hung Background and Objective:, Polymorphonuclear leukocytes are the major source of leukotriene B4, which is synthesized via the 5-lipoxygenase pathway. Activation of the 5-lipoxygenase pathway is regulated by intracellular calcium and the phosphorylation of p38 mitogen-activated protein kinase (MAPK). The impact of areca nut extracts on the biosynthesis of leukotriene B4 by human polymorphonuclear leukocytes was evaluated, and some of the possible mechanisms underlying the responses were examined. Material and Methods:, Polymorphonuclear leukocytes were treated with various concentrations of areca nut extracts. The concentrations of leukotriene B4 released into the supernatants were evaluated using enzyme immunoassay. The phosphorylation of p38 MAPK was monitored using immunoblotting, and the cytosolic calcium kinetics were assessed fluorometrically using Fura-2. Results:, Exposure of polymorphonuclear leukocytes to areca nut extracts led to a dose-dependent increase in the production of leukotriene B4, with levels peaking at 30 min and decreasing thereafter. Areca nut extracts enhanced the phosphorylation of p38 MAPK, an enzyme known to activate 5-lipoxygenase. Incubation with areca nut extracts also resulted in a rapid elevation of intracellular calcium concentrations in polymorphonuclear leukocytes. The induction of leukotriene B4 by areca nut extracts was suppressed with the p38 MAPK inhibitor, SB203580, or with the intracellular calcium chelator, BAPTA-AM. Conclusion:, The interaction of areca nut extracts with polymorphonuclear leukocytes activated the arachidonic acid metabolic cascade. Incubation of polymorphonuclear leukocytes with areca nut extracts resulted in the activation of intracellular events, such as phosphorylation of p38 MAPK and Ca2+ mobilization, involved in the release of pro-inflammatory lipid mediators. The results of this study emphasize the potential importance of polymorphonuclear leukocytes as a source of leukotriene B4, which may modulate the inflammatory response in areca chewers. [source] Differential platelet-activating factor synthesis by monocytes and polymorphonuclear leukocytes from subjects with localized aggressive periodontitisJOURNAL OF PERIODONTAL RESEARCH, Issue 3 2007C. R. Shin Background and Objective:, Platelet-activating factor is elevated in localized aggressive periodontitis. We previously demonstrated that the elevated level of platelet-activating factor in localized aggressive periodontitis is at least partially attributable to low levels of platelet-activating factor acetylhydrolase, the enzyme that catabolizes platelet-activating factor. The objective of this study was to determine if platelet-activating factor synthesis was also elevated in localized aggressive periodontitis. To test this, platelet-activating factor synthesis was quantified in the monocytes and polymorphonuclear neutrophils of periodontally healthy patients and of subjects with localized aggressive periodontitis. Material and Methods:, Cells were labeled with [3H]acetate and treated with vehicle or stimulated with calcium ionophore A23187. Platelet-activating factor was extracted and quantified by scintillation counting. Results:, For both subject groups, resting monocytes and polymorphonuclear neutrophils produced platelet-activating factor, and calcium ionophore A23187 stimulated platelet-activating factor production in both cell types. However, calcium ionophore A23187-activated monocytes from subjects with localized aggressive periodontitis produced less platelet-activating factor than did activated periodontally healthy monocytes (p < 0.0001), suggesting an aberrant calcium ionophore A23187 response in monocytes from subjects with localized aggressive periodontitis. Indeed, when the data were expressed as fold induction of platelet-activating factor synthesis in response to calcium ionophore A23187, monocytes from subjects with localized aggressive periodontitis exhibited only a fourfold increase in platelet-activating factor synthesis, whereas calcium ionophore A23187-stimulated monocytes from periodontally healthy, chronic periodontitis and generalized aggressive periodontitis subjects produced ,,12 times more platelet-activating factor than did resting monocytes. In contrast, both resting and activated localized aggressive periodontitis polymorphonuclear neutrophils synthesized more platelet-activating factor than did periodontally healthy polymorphonuclear neutrophils. Conclusion:, These data suggest that high levels of platelet-activating factor in subjects with localized aggressive periodontitis result from both increased synthesis and reduced catabolism. While localized aggressive periodontitis polymorphonuclear neutrophils contribute to increased platelet-activating factor mass through synthesis, the contribution of monocytes is probably the result of reduced catabolism by platelet-activating factor acetylhydrolase. [source] Different distribution of immunocompetent cells in the dentogingival junction during root formation in rat molarsJOURNAL OF PERIODONTAL RESEARCH, Issue 1 2003Hiroshi Tamura The distribution of immunocompetent cells in the dentogingival junction of rat molars during root formation was investigated by immunocytochemistry using antibodies to class II major histocompatibility complex (MHC) molecules (OX6-antibody) and monocyte/macrophage lineage cells (ED1-antibody) as well as by histochemical reaction for periodic acid,Schiff (PAS). Two portions (the junctional epithelium in the mesial gingiva of the first molar, and the interdental gingiva between the first and second molars) were selected for observations. At the eruption stage of the first molar (16,18 days after birth), OX6-positive cells, dendritic or oval in shape, were abundantly distributed in the connective tissue between the oral epithelium and tooth germ. Positive cells with slender cell processes were also found beneath the ameloblast layer. At the commencement stage of the first molar occlusion (24,28 days after birth), numerous OX6-positive cells displaying a dendritic fashion existed preferentially in the mesial gingiva, but were fewer in the interdental gingiva. In contrast, the interdental gingiva showed a denser distribution of ED1-positive cells and PAS-reactive polymorphonuclear leukocytes (PMLs) than the mesial gingiva. At the completion stage of root formation (100,120 days after birth), the OX6-immunopositive cells invaded the deeper position of the mesial gingiva with the downgrowth of the epithelium; they had a considerably higher cell density compared with those in the interdental gingiva where PAS-reactive PMLs persisted. These findings indicated that the immunocompetent cells showed a region-specific distribution and cell density by their roles in immune response. [source] Isolation of eriocitrin (eriodictyol 7- O -rutinoside) as an arachidonate lipoxygenase inhibitor from Lumie fruit (Citrus lumia) and its distribution in Citrus speciesJOURNAL OF THE SCIENCE OF FOOD AND AGRICULTURE, Issue 1 2007Yoichi Nogata Abstract An inhibitory compound acting against rat platelet 12-lipoxygenase was isolated from the peel of Lumie fruit (Citrus lumia) by activity-guided separation. It was identified as eriocitrin (eriodictyol 7- O -rutinoside) by spectroscopic analyses. Eriocitrin inhibited 5-lipoxygenase (IC5029.1 µmol L,1) from rat peritoneal polymorphonuclear leukocytes in addition to 12-lipoxygenase (IC5022.3 µmol L,1). Its aglycone, eriodictyol (5,7,3,, 4,-tetrahydroxyflavanone), was a much more potent inhibitor of both 12-lipoxygenase (IC500.07 µmol L,1) and 5-lipoxygenase (IC500.20 µmol L,1). It also inhibited the production of leukotriene B4 in intact peritoneal polymorphonuclear leukocytes stimulated with calcium ionophore A23187 (IC5012.7 µmol L,1). The distribution of eriocitrin in 39 citrus fruits was investigated by high-performance liquid chromatography analysis. Lumie, eureka lemon (Citrus limon), Sambokan (Citrus sulcata), Sudachi (Citrus sudachi) and Koji (Citrus leiocarpa) fruits were found to contain high levels of eriocitrin in both peel and juice vesicles. Copyright © 2006 Society of Chemical Industry [source] Effect of cigarette smoke extract on the polymorphonuclear leukocytes chemiluminescence: influence of a filter containing glutathioneLUMINESCENCE: THE JOURNAL OF BIOLOGICAL AND CHEMICAL LUMINESCENCE, Issue 2 2005B. Zappacosta Abstract Cigarette smoking is known to be a risk factor for several chronic and neoplastic diseases. Many compounds formed by cigarette burning, ranging from particulate materials to water solutes and gaseous extracts, are considered to be noxious agents, and many biochemical and molecular mechanisms have been proposed for the toxic effects of cigarette smoke. The oral cavity and the upper respiratory tract represent the first contact areas for smoke compounds; even a single cigarette can produce marked effects on some components of the oral cavity, either chemical compounds, such as glutathione and enzymes, or cellular elements, such as polymorphonuclear leukocytes. Several studies suggest a protective role of glutathione against the noxious effects of tobacco smoke; the sulphydril groups of glutathione, in fact, could react with some smoke products, such as unsaturated aldehydes, leading to the formation of harmless intermediate compounds and simultaneously preventing the inactivation of metabolically essential molecules, such as some enzymes. In this paper we analyse the effect of a filter containing glutathione on the respiratory burst of polymorphonuclear leukocytes exposed to aqueous extract of cigarette smoke, measuring their chemiluminescence activity. The results of this paper indicate that the GSH--containing filter has a likely protective effect against the inhibition of cigarette smoke extract on polymorphonuclear leukocyte activity. Copyright © 2005 John Wiley & Sons, Ltd. [source] Effect of aqueous cigarette smoke extract on the chemiluminescence kinetics of polymorphonuclear leukocytes and on their glycolytic and phagocytic activityLUMINESCENCE: THE JOURNAL OF BIOLOGICAL AND CHEMICAL LUMINESCENCE, Issue 5 2001Bruno Zappacosta Abstract Water-soluble extracts of cigarette smoke are easily formed in some body compartments, such as saliva or fluid lining alveolar spaces, and can act on both cellular and extracellular compartments. In this paper we have analysed the effect of aqueous smoke extract on some metabolic and functional aspects of polymorphonuclear leukocytes. In particular, the following cellular aspects were studied: chemiluminescence, glycolysis, membrane fluidity and microscopic interaction with zymosan particles. While chemiluminescence and glycolytic activity are highly inhibited, no effect of smoke extract on membrane fluidity was observed. Moreover, the response of luminol-dependent chemiluminescence was significantly delayed, while that of lucigenin-dependent chemiluminescence was anticipated. Furthermore, the phagocytic ability of neutrophils pretreated with aqueous smoke extract was also significantly hindered. All these results might indicate that the finely tuned activity of polymorphonuclear leukocytes is somehow hampered by the aqueous extract of cigarette smoke in a way which makes these cells less effective against bacteria and more noxious towards surrounding tissues. Copyright © 2001 John Wiley & Sons, Ltd. [source] Detection of serotype k Streptococcus mutans in Thai subjectsMOLECULAR ORAL MICROBIOLOGY, Issue 5 2009J. Lapirattanakul Introduction:,Streptococcus mutans, known to be a pathogen of dental caries as well as bacteremia and infective endocarditis, is classified into four serotypes, c, e, f and k, based on the structures of serotype-specific polysaccharides. Serotype k was recently designated using blood isolates from Japanese subjects and such strains are considered to be virulent in the bloodstream. The purpose of the present study was to analyse the serotype distribution of strains isolated from Thai subjects and determine whether serotype k strains were present. Methods:, A total of 250 S. mutans strains were isolated from 50 Thai subjects, and serotypes of all strains were determined. Then, molecular and biological analyses were carried out for serotype k strains. Results:, Immunodiffusion and polymerase chain reaction analyses showed that serotype c was the most prevalent (70%), followed by serotypes e (22.8%), f (4.4%) and k (2.8%), which indicated that serotype k S. mutans strains occurred in Thai individuals at a similar rate to that previously reported for Japanese and Finnish populations. Molecular analyses of the seven serotype k strains showed extremely low expression of rgpE, which is related to glucose side-chain formation in serotype-specific rhamnose-glucose polymers, similar to previous reports for those other populations. In addition, analysis of the biological properties of the seven serotype k strains demonstrated low levels of sucrose-dependent adhesion, cellular hydrophobicity, dextran-binding activity and phagocytosis susceptibility by human polymorphonuclear leukocytes, which are characteristics similar to those of serotype k strains previously isolated in Japan. Conclusion:, Our results indicate the possibility of a worldwide prevalence of serotype k strains with properties in common with those of previously reported strains. [source] Functional characteristics of antibodies induced by Arg-gingipain (HRgpA) and Lys-gingipain (Kgp) from Porphyromonas gingivalisMOLECULAR ORAL MICROBIOLOGY, Issue 4 2001T. Nakagawa Arginine-specific gingipain (HRgpA) and lysine-specific gingipain (Kgp), enzymes produced by Porphyromonas gingivalis, may be candidates for an anti,P. gingivalis vaccine. The purpose of our study was to determine whether HRgpA and Kgp have opsonic target sites and whether these sites are available and accessible on intact P. gingivalis cells. Rabbits were used to generate polyclonal antibodies to both proteins. Animals were immunized and immunoglobulin G (IgG) fractions were isolated from preimmune and immune sera. Functional characteristics of the antibodies were assessed by determining antibody titers by enzyme-linked immunosorbent assay (ELISA), generating Western immunoblots, and measuring antibody enhancement of P. gingivalis opsonization, phagocytosis and killing by polymorphonuclear leukocytes (PMN) of intact cells of strains of P. gingivalis representative of the four serotypes. Strains studied included 33277 (serotype A), A7A1,28 (serotype B), W50 (serotype C) and 381 (serotype D). Both HRgpA and Kgp induced high titers of IgG antibody. Anti-HRgpA and anti-Kgp bound to both HRgpA and Kgp demonstrating a large proportion of shared antigenic epitopes. The two antibodies bound equally well to all four P. gingivalis serotypes with titers ranging from 77 to 205 ELISA units when compared to preimmune IgG set at 1 ELISA unit. The immunoblot patterns of binding of the two antibodies to HRgpA and Kgp and to sonicates of the four P. gingivalis serotypes were virtually identical. Both antibodies detected components in HRgpA at 27, 35 and 45 kDa and in Kgp at 27, 32, 35, 40 and 55 kDa. The antibodies also detected components at or near these same positions in addition to multiple high molecular mass components in the cell sonicates of P. gingivalis. Both proteins induced antibodies that significantly enhanced opsonization as assessed by chemiluminescence, with values ranging from 130 mV to 375 mV for anti-HRgpA IgG and from 240 mV to 475 mV for anti-Kgp IgG. Both antibodies significantly enhanced PMN-mediated bacterial killing of the four P. gingivalis serotypes, although the percentage of killing varied among the serotypes (24,81% for anti-HRgpA and 37,89% for anti-Kgp). Thus, both HRgpA and Kgp express opsonic target sites and induce high titers of antibodies that opsonize and enhance killing of all four serotypes of P. gingivalis. These two proteins appear to be potential candidate antigens for an anti,P. gingivalis vaccine. [source] Fimbriae of Porphyromonas gingivalis induce opsonic antibodies that significantly enhance phagocytosis and killing by human polymorphonuclear leukocytesMOLECULAR ORAL MICROBIOLOGY, Issue 3 2001Q. Fan Porphyromonas gingivalis has been strongly implicated in the pathogenesis of human periodontitis. Fimbriae mediate adherence and colonization of the oral cavity by this organism and may, therefore, have potential for use as antigen in an anti,P. gingivalis vaccine. The purpose of our study was to determine whether P. gingivalis fimbriae have opsonic target sites and whether they are accessible on the cell surfaces and cross-reactive among P. gingivalis fimbrial types and serotypes. Rabbits were immunized with a vaccine. The antiserum reacted with a 43-kDa fimbrillin monomer and a 43-kDa component in whole-cell sonicates of P. gingivalis 33277, but it showed only very weak reactivity in the 43-kDa region of Western blots of a whole-cell sonicate of strain DPG3, a mutant that does not express functional fimbriae. The antibody enhanced chemiluminescence approximately six-fold relative to preimmune serum values and significantly enhanced phagocytosis and killing of P. gingivalis 33277 by human polymorphonuclear leukocytes. Peak opsonic activity was observed at week 6 followed by a plateau that remained until week 16. The fimbria-deficient mutant DPG3 did not bind antifimbrial antibody and was not opsonized, whereas strain 381, the parent of the mutant, was opsonized. The specific antibody bound to and opsonized P. gingivalis strains 33277 and 381 (fimbria type I) but not W50, A7A-1-28, 9-14K-1 or FAY-19M-1 (fimbrial types II,V). Specific antibody bound to strain 2561 (fimbrial type I) but, as assessed by chemiluminescence, did not opsonize it. While fimbriae have opsonic target sites that are accessible on P. gingivalis cell surfaces, the relevant opsonic target sites do not appear to be shared across serotypes or fimbrial types. Thus, a vaccine containing, as antigen, fimbrial protein from a single P. gingivalis strain would likely be ineffective against infections by P. gingivalis strains expressing other fimbrial types. [source] | ||||||||||||||||