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Inflammatory Conditions (inflammatory + condition)
Kinds of Inflammatory Conditions Selected AbstractsCritical determinants of the interactions of capsule-expressing Neisseria meningitidis with host cells: the role of receptor density in increased cellular targeting via the outer membrane Opa proteinsCELLULAR MICROBIOLOGY, Issue 10 2005Christopher J. Bradley Summary Neisseria meningitidis capsule is an important virulence determinant required for survival in the blood but is reportedly involved in inhibiting cellular interactions mediated by meningococcal outer membrane adhesins. However, evidence from our previous studies suggested that target receptor density on host cells may determine whether or not capsulate bacteria can adhere via outer membrane proteins such as Opa. To confirm this and evaluate the impact of capsulation on bacterial interactions, we used Opa+ and Opa, derivatives of capsulate and acapsulate meningococcal isolates and transfected cell lines expressing CEACAM1, a receptor targeted by Opa proteins. To assess the extent and rate of cell association, subpopulations of stably transfected Chinese hamster ovary cells with different receptor levels were derived. A quantitative correlation of CEACAM1 levels and Opa-dependent binding of both capsulate and acapsulate bacteria was demonstrated, which was accelerated at high receptor densities. However, it appears that invasion by Opa+ capsulate bacteria only occurs when a threshold level of CEACAM density has been reached. Target cells expressing high levels of CEACAM1 (MFI c. 400) bound threefold more, but internalized 20-fold more Opa+ capsulate bacteria than those with intermediate expression (MFI c. 100). No overall selection of acapsulate phenotype was observed in the internalized population. These observations confirm that capsule may not be an adequate barrier for cellular interactions and demonstrate the role of a host factor that may determine capsulate bacterial invasion potential. Upregulation of CEACAMs, which can occur in response to inflammatory cytokines, could lead to translocation of a small number of fully capsulate bacteria across mucosal epithelium into the bloodstream sufficient to cause a rapid onset of disseminated disease. Thus the data also suggest a novel rationale for the epidemiological observations that individuals with prior infectious/inflammatory conditions carry a high risk of invasive meningococcal disease. [source] Effect of crown fracture on the surrounding periodontiumDENTAL TRAUMATOLOGY, Issue 3 2008Janaína Cristina Gomes To reach the long axis of the tooth, an impact device was applied to eight teeth of four adult dogs to produce trauma. Crown fractures involving the enamel and dentin, with or without pulpar exposure and without dislocation, mobility or gingival bleeding were analyzed within the post-trauma periods of 30 min, 1, 3, and 7 days. The force of impact that resulted in coronary fracture, although dissipated at the time of fracture, reverberated in the surrounding periodontium and may generate not only light histological alterations with a rapid re-establishment of the tissues, but also an intense inflammatory condition required as long as 7 days to clear up. The gravity of these inflammatory reactions unleashed in these teeth's periapical tissues depends on the absorption of impact by the periodontal structures and the individual susceptibility of each organism. [source] Interferon regulatory factor-3 activation, hepatic interferon-stimulated gene expression, and immune cell infiltration in hepatitis C virus patients,HEPATOLOGY, Issue 3 2008Daryl T.-Y. Interferon regulatory factor-3 (IRF-3) activation directs ,/, interferon production and interferon-stimulated gene (ISG) expression, which limits virus infection. Here, we examined the distribution of hepatitis C virus (HCV) nonstructural 3 protein, the status of IRF-3 activation, and expression of IRF-3 target genes and ISGs during asynchronous HCV infection in vitro and in liver biopsies from patients with chronic HCV infection, using confocal microscopy and functional genomics approaches. In general, asynchronous infection with HCV stimulated a low-frequency and transient IRF-3 activation within responsive cells in vitro that was associated with cell-to-cell virus spread. Similarly, a subset of HCV patients exhibited the nuclear, active form of IRF-3 in hepatocytes and an associated increase in IRF-3 target gene expression in hepatic tissue. Moreover, ISG expression profiles formed disease-specific clusters for HCV and control nonalcoholic fatty liver disease patients, with increased ISG expression among the HCV patients. We identified the presence of T cell and plasmacytoid dendritic cell infiltrates within all biopsy specimens, suggesting they could be a source of hepatic interferon in the setting of hepatitis C and chronic inflammatory condition. Conclusion: These results indicate that HCV can transiently trigger IRF-3 activation during virus spread and that in chronic HCV, IRF-3 activation within infected hepatocytes occurs but is limited. (HEPATOLOGY 2007.) [source] Inflammatory cytokines modulate chemokine production patterns of HepG2 cells toward initially inclined directionHEPATOLOGY RESEARCH, Issue 5 2009Tomohiko Ohashi Aim:, Human hepatocytes are known to express an array of inflammatory cytokines and chemokines. In this study, we examined the potential roles of hepatocytes in regulating immune responses in the liver, by assessing the induction of Th1- or Th2-specific chemokines in HepG2 cells after various inflammatory stimulations. Methods:, HepG2 cells were stimulated with IL-1,, IFN-,, IL-4, IL-10, and/or CCL2, harvested at several time points, and served for the analyses of cytokine/chemokine mRNA expressions by semi-quantitative RT-PCR. Results:, (i) IL-1, up-regulated mRNA levels of CXCL8, CXCL10, and CCL2. IFN-, increased those of CXCL9, CXCL10, and CCL5, while IL-4 or IL-10 had no effect. (ii) Addition of IL-4 to the culture of IFN-,-stimulated cells, down-regulated CXCL9 and CXCL10 mRNA levels. (iii) Addition of IFN-, to the culture of IL-1,-stimulated cells, further up-regulated CXCL9 and CXCL10 mRNA levels. Addition of IL-4 decreased CXCL8 and CXCL10 levels, and increased CCL2 level in IL-1,-stimulated cells. (iv) CCL2 induced IL-4 mRNA expression. Conclusions:, IFN-, augmented mRNA expression of Th1-specific chemokines (CXCL9 and CXCL10) in HepG2 cells. IL-4 had no effect on those of Th2-spesific chemokines (CCL17 and CCL22); however, it was supposed to augment Th2 response indirectly through the induction of CCL2 under the inflammatory condition. The findings suggest that hepatocytes have ability to promote immune responses in the liver toward the direction, initially determined by the cytokine balances in the local inflammatory region. [source] Abnormal Pap smears in inflammatory bowel diseaseINFLAMMATORY BOWEL DISEASES, Issue 8 2008Sunanda Kane MD Abstract Inflammatory bowel disease (IBD) is a chronic inflammatory condition that is frequently treated with immunomodulators. Previous work has demonstrated an increased risk for abnormal cervical cytology in women treated with chronic immunosuppression, due mainly to human papillomavirus. This review summarizes the data known for this relationship in women with IBD, and management strategies for patients found to have abnormal cervical cytology. (Inflamm Bowel Dis 2008) [source] Sebaceous Carcinoma of the Eyelid: Analogy to Extramammary Paget's DiseaseJOURNAL OF CUTANEOUS PATHOLOGY, Issue 1 2005J.B. Lee We present a 69-year-old woman with a sebaceous carcinoma of the left upper eyelid, which originated from the Meibomian gland of the tarsal plate. The intraepidermal extension involved not only the conjunctival epithelium but also the overlying skin with subsequent extension into the dermis. The discussion will include diagnostic, both clinical and microscopic, considerations along with comparison to mammary Paget's disease. Just as mammary Paget's disease, which originates from the glands in the dermis eventuating in the seeding of the overlying epidermis, so too does sebaceous carcinoma of the eyelid. Accordingly, just as mammary Paget's disease is often misdiagnosed as an inflammatory condition, so too is sebaceous carcinoma. [source] Vaccine-associated granulomatous inflammation and melanin accumulation in Atlantic salmon, Salmo salar L., white muscleJOURNAL OF FISH DISEASES, Issue 1 2005E O Koppang Abstract The purpose of this study was to investigate the nature of variably sized pigmented foci encountered in fillets of farmed Atlantic salmon, Salmo salar L. The material was sampled on the fillet production line and on salmon farms from fish with an average size of 3 kg from various producers. The fish had been routinely vaccinated by injection. Gross pathology, histology, immunohistochemistry using antisera against major histocompatibility complex (MHC) class II , chain and transmission electron microscopy (TEM) were used to characterize the changes. Macroscopically, melanized foci were seen penetrating from the peritoneum deep into the abdominal wall, sometimes right through to the skin, and also embedded in the caudal musculature. Histological investigation revealed muscle degeneration and necrosis, fibrosis and granulomatous inflammation containing varying numbers of melano-macrophages. Vacuoles, either empty or containing heterogeneous material, were frequently seen. The presence of abundant MHC class II+ cells indicated an active inflammatory condition. TEM showed large extracellular vacuoles and leucocytes containing homogeneous material of lipid-like appearance. The results showed that the melanized foci in Atlantic salmon fillet resulted from an inflammatory condition probably induced by vaccination. The described condition is not known in wild salmon and in farmed salmon where injection vaccination is not applied. [source] Inflammation: A new candidate in modulating adult neurogenesisJOURNAL OF NEUROSCIENCE RESEARCH, Issue 6 2008Sulagna Das Abstract Any pathological perturbation to the brain provokes a cascade of molecular and cellular events, which manifests in the form of microglial activation and release of various proinflammatory molecules. This eventually culminates in a profound neuroinflammatory reaction that characterizes the brain's response to stress, injury, or infection. The inflammatory cascade is an attempt by the system to eliminate the challenge imposed on the brain, clear the system of the dead and damaged neurons, and rescue the normal functioning of this vital organ. However, during the process of microglial activation, the proinflammatory mediators released exert certain detrimental effects, and neural stem cells and progenitor cells are likely to be affected. Here we review how the proliferation, maturation, and migration of the neural stem cells are modulated under such an inflammatory condition. The fate of the noncommitted neural stem cells and its differentiation potency are often under strict regulation, and these proinflammatory mediators seem to disrupt this critical balance and finely tune the neurogenesis pattern in the two niches of neurogenesis, the subventricular zone and the subgranular zone of the hippocampus. Moreover, the migration ability of these stem cells, which is important for localization to the proper site, is also affected in a major way by the chemokines released following inflammation. © 2007 Wiley-Liss, Inc. [source] Cervical sympathectomy causes alveolar bone loss in an experimental rat modelJOURNAL OF PERIODONTAL RESEARCH, Issue 6 2009Y. Kim Background and Objective:, Periodontal disease, a pathological destructive inflammatory condition, is characterized by alveolar bone loss. Recent studies have suggested a correlation between the sympathetic nervous system and bone remodeling. To confirm the importance of the sympathetic nervous system in bone resorption, we investigated the effects of superior cervical ganglionectomy and oral challenge with Porphyromonas gingivalis on alveolar bone loss in rats. Material and Methods:, Rats were divided into three groups: group A underwent a sham operation as the control group; group B underwent superior cervical ganglionectomy; and group C underwent a sham operation and oral challenge with P. gingivalis. Horizontal alveolar bone loss was evaluated by measuring the distance between the cemento-enamel junction and the alveolar bone crest. Cytokine gene expression in the gingival tissues was assessed using reverse transcription,polymerase chain reaction analyses. The furcation areas of the mandibular molars were examined histologically. Results:, Both superior cervical ganglionectomy and oral challenge with P. gingivalis resulted in accelerated alveolar bone loss. Gingival tissues in the superior cervical ganglionectomy group showed increased expression of the cytokines interleukin-1alfa, tumor necrosis factor-alfa and interleukin-6. The density of neuropeptide Y-immunoreactive fibers was decreased following superior cervical ganglionectomy. Osteoclasts were observed in the superior cervical ganglionectomy and P. gingivalis- challenged groups. Conclusion:, Both superior cervical ganglionectomy and oral challenge with P. gingivalis induced alveolar bone loss. These results provide new information on the occurrence of alveolar bone loss, in that both oral challenge with P. gingivalis and superior cervical ganglionectomy are important accelerating factors for alveolar bone loss. Thus, we suggest that the sympathetic nervous system is linked with the prevention of alveolar bone loss. [source] Role of systemic and local administration of selective inhibitors of cyclo-oxygenase 1 and 2 in an experimental model of periodontal disease in ratsJOURNAL OF PERIODONTAL RESEARCH, Issue 2 2009C. M. Queiroz-Junior Background and Objective:, Periodontal disease is an inflammatory condition of tooth-supporting tissues. Arachidonic acid metabolites have been implicated in development of periodontal disease, especially those derived from the cyclo-oxygenase (COX) pathway. This study investigated the role of inhibitors of cyclo-oxygenases (COX-1 and COX-2) in a model of periodontal disease in rats. Material and Methods:, A ligature was placed around the molar of rats. Losses of fiber attachment and of alveolar bone were measured morphometrically in histologically prepared sections. Infiltration of cells into gingival tissue surrounding the ligated tooth was also determined. Results:, Systemic and local administration of non-selective and selective COX-2 inhibitors, preventively, resulted in significant reduction of the losses of fiber attachment and alveolar bone, as well as decreased leukocyte numbers in gingival tissue. Preventive selective inhibition of COX-1 was as effective as COX-2 inhibition in reducing local fiber attachment loss and cell migration, but did not prevent alveolar bone loss. Conclusion:, Our results provide evidence for participation of COX-1 and COX-2 in early stages of periodontal disease in rats. Furthermore, local administration of COX inhibitors reduced the signs of periodontal disease to the same extent as systemic treatment. Therapeutic approaches incorporating locally delivered anti-inflammatory drugs could be of benefit for patients suffering from periodontal disease. [source] Acute pancreatitis in dogsJOURNAL OF VETERINARY EMERGENCY AND CRITICAL CARE, Issue 4 2003Jennifer L. Holm DVM Abstract Objective: To summarize current information regarding severity assessment, diagnostic imaging, and treatment of human and canine acute pancreatitis (AP). Human-based studies: In humans, scoring systems, advanced imaging methods, and serum markers are used to assess the severity of disease, which allows for optimization of patient management. The extent of pancreatic necrosis and the presence of infected pancreatic necrosis are the most important factors determining the development of multiple organ failure (MOF) and subsequent mortality. Considerable research efforts have focused on the development of inexpensive, easy, and reliable laboratory markers to assess disease severity as early as possible in the course of the disease. The use of prophylactic antibiotics, enteral nutrition, and surgery have been shown to be beneficial in certain patient populations. Veterinary-based studies: The majority of what is currently known about naturally occurring canine AP has been derived from retrospective evaluations. The identification and development of inexpensive and reliable detection kits of key laboratory markers in dogs with AP could dramatically improve our ability to prognosticate and identify patient populations likely to benefit from treatment interventions. Treatment remains largely supportive and future studies evaluating the efficacy of surgery, nutritional support and other treatment modalities are warranted. Data sources: Current human and veterinary literature. Conclusions: Pancreatitis can lead to a life-threatening severe systemic inflammatory condition, resulting in MOF and death in both humans and dogs. Given the similarities in the pathophysiology of AP in both humans and dogs, novel concepts used to assess severity and treat people with AP may be applicable to dogs. [source] The pathology and pathogenesis of retinal vasculitisNEUROPATHOLOGY & APPLIED NEUROBIOLOGY, Issue 4 2003E. H. Hughes Retinal vasculitis is a rare, but potentially blinding intraocular inflammatory condition with diverse aetiology. Although commonly idiopathic, it has a strong association with systemic inflammatory diseases known to involve other areas of the central nervous system, most notably Behcet's disease, sarcoidosis, systemic lupus erythematosis and multiple sclerosis. This article describes the clinicopathologic features of retinal vasculitis and its visually damaging sequelae, reviewing available human histopathologic studies and work with experimental models to discuss the pathogenesis and immunopathology. Evidence indicates that noninfective retinal vasculitis is an autoimmune condition that may be induced by antecedent infection with microbes cross,reacting with putative autoantigens, influenced by genetic susceptibility of both HLA associations and cytokine polymorphisms. The growing understanding of the cellular mechanisms involved in the effector immune response is already providing a rationale for more specific therapeutic approaches. [source] Urethral Corpus Spongiosum Amyloidosis Presenting with Urethrorrhagia During ErectionTHE JOURNAL OF SEXUAL MEDICINE, Issue 10 2009Luigi Cormio MD ABSTRACT Introduction., Urethral amyloidosis is a rare, probably inflammatory condition usually presenting with hematuria and obstructive urinary symptoms, thus mimicking urethral malignancy. After histological confirmation of the diagnosis, treatment can be expectant or symptomatic. Aim., To report an unusual cause of urethrorrhagia occurring only during erection in an otherwise healthy man. Methods., A 30-year-old man presented with a 5-month history of urethrorrhagia occurring only during erection, and with a painless palpable nodule in his penile urethra clearly visible on urethral US and magnetic resonance imaging, but not on urethroscopy. Results., The patient underwent wide surgical excision of the urethral nodule and grafting of the urethral defect with a pedicled preputial flap. Histological examination revealed isolated amyloid of urethral corpus spongiosum. Conclusions., Isolated urethrorrhagia during erection and without urinary symptoms can be the presenting sign of urethral amyloidosis involving corpus spongiosum rather than the urethral lumen; in such cases, surgical exploration, wide urethral excision and grafting are mandatory. Cormio L, Sanguedolce F, Pentimone S, Perrone A, Annese P, Turri FP, Bufo P, and Carrieri G. Urethral corpus spongiosum amyloidosis presenting with urethrorrhagia during erection. J Sex Med 2009;6:2915,2917. [source] Degranulation of Mast Cells Provokes a Massive Inflammatory Reaction in the Tympanic Membrane,THE LARYNGOSCOPE, Issue 7 2001Per Olof Eriksson MD Abstract Objective The pars flaccida is extremely rich in mast cells. On stimulation the mast cells release preformed and de novo synthesized inflammatory substances. The purpose of this study was to examine how these mast cell substances provoke inflammatory changes in the tympanic membrane. Study Design In vivo, murine model. Methods In a rat model, the mast cell secretagogue compound 48/80 was applied locally to the tympanic membrane on 4 consecutive days and the ensuing inflammatory changes were evaluated by otological, light, and electron microscopy 3, 6, 9, 12, 18, 24, 36, and 48 hours and 4, 6, and 8 days later. Results Degranulation of the mast cells occurred within 3 hours of applying compound 48/80. Release of the mast cell substances coincided with an inflammatory event characterized by a two-stage reaction: an edema stage, peaking 6 hours after application, followed by a massive invasion of inflammatory cells, peaking at 24 and 48 hours. Pars flaccida and pars tensa were both involved, pars flaccida showing the earliest changes. Pars tensa exhibited the same biphasic reaction as pars flaccida, but approximately 6 hours later. Conclusions The mast cells of the pars flaccida have the capacity to elicit an intense inflammation of the tympanic membrane. The biphasic reaction pattern resembles that observed in experimental otitis media, suggesting involvement of the mast cells in this inflammatory condition of the middle ear. [source] Asthma and oral health: a reviewAUSTRALIAN DENTAL JOURNAL, Issue 2 2010MS Thomas Abstract Asthma is a chronic inflammatory condition that causes the airways to constrict and produce excess mucus, making breathing difficult. It is characterized by the obstruction of airflow which is variable over a short period of time. This condition is reversible, either spontaneously or can be controlled with the help of drugs. Asthma medication comprises bronchodilators, corticosteroids and anticholinergic drugs. Most of these drugs are inhaled using various forms of inhalers or nebulizers. The effect of these drugs on oral health is the subject of debate among dental practitioners. Patients taking asthma medication may be at risk of dental caries, dental erosion, periodontal diseases and oral candidiasis. Hence, patients with bronchial asthma on medication should receive special prophylactic attention. This article reviews the correlation between asthma and oral health, and suggests various measures to counter possible oral health problems related to asthma. [source] Regulation of the human taurine transporter by TNF-, and an anti-inflammatory function of taurine in human intestinal Caco-2, cellsBIOFACTORS, Issue 1-4 2004Tetsunosuke Mochizuki Abstract We investigated whether or not the inflammatory cytokines affect the activity of taurine transporter (TAUT) in human intestinal Caco-2, cells. Among the cytokines, tumor necrosis factor ,(TNF-,) markedly augmented the TAUT activity. A kinetic analysis of the TAUT activity in TNF-,-treated Caco-2 cells suggests that this up-regulation was associated with both an increase in the amount of TAUT and an increase in its affinity. Considering these results, it seems that intracellular taurine plays a role in the intestinal epithelial cells under such an inflammatory condition as that caused by an excessive amount of TNF-, secreted by macrophages. To verify this hypothesis, we examined the effect of taurine on inflamed intestinal cells by using a co-culture system of Caco-2 cells with human macrophage-like THP-1 cells. The result shows that taurine significantly repressed the damage to Caco-2 cells caused by TNF-, secreted by THP-1 cells. Thus, taurine may be a useful substance against intestinal inflammation. [source] Clindamycin and rifampicin combination therapy for hidradenitis suppurativaBRITISH JOURNAL OF DERMATOLOGY, Issue 5 2006C.O. Mendonça Summary Background, Hidradenitis suppurativa (HS) is a chronic inflammatory condition affecting apocrine gland-bearing areas of the skin. There is currently no satisfactory treatment. Objectives, To assess the efficacy of a 10-week course of combination clindamycin 300 mg twice daily and rifampicin 300 mg twice daily in the treatment of HS. Methods, Patients who had received combination therapy with clindamycin and rifampicin for HS at one U.K. Dermatology Centre between the years 1998 and 2003 were identified from pharmacy records. Their records were analysed retrospectively. Results, Fourteen patients with HS had received treatment with combination therapy. Eight of these patients achieved remission and a further two achieved remission when minocycline was substituted for clindamycin. Four patients were unable to tolerate therapy. Conclusions, This small retrospective study indicates that combination therapy with clindamycin and rifampicin may be effective for HS. However, there is a need for a placebo-controlled trial. [source] Inhibition of caspase-dependent spontaneous apoptosis via a cAMP-protein kinase A dependent pathway in neutrophils from sickle cell disease patientsBRITISH JOURNAL OF HAEMATOLOGY, Issue 1 2007Nicola Conran Summary Sickle cell disease (SCD) is a chronic inflammatory condition characterized by high leucocyte counts, altered cytokine levels and endothelial cell injury. As the removal of inflammatory cells by apoptosis is fundamental for the resolution of inflammation, we aimed to determine whether the leucocyte apoptotic process is altered in SCD. Neutrophils from SCD individuals showed an inhibition of spontaneous apoptosis when cultured in vitro, in the presence of autologous serum for 20 h. Intracellular cyclic adenosine monophosphate (cAMP) levels were approximately twofold increased in SCD neutrophils; possible cAMP-upregulating factors present in SCD serum include interleukin-8, granulocyte-macrophage colony-stimulating factor and prostaglandin. Accordingly, co-incubation of SCD neutrophils with KT5720, a cAMP-dependent protein kinase (PKA) inhibitor, abrogated increased SCD neutrophil survival. Caspase-3 activity was also significantly diminished in SCD neutrophils cultured for 16 h and this activity was restored when cells were co-incubated with KT5720. BIRC2 (encoding cellular inhibitor of apoptosis protein 1, cIAP1), MCL1 and BAX expression were unaltered in SCD neutrophils; however, BIRC3 (encoding the caspase inhibitor, cIAP2), was expressed at significantly higher levels. Thus, we report an inhibition of spontaneous SCD neutrophil apoptosis that appears to be mediated by upregulated cAMP-PKA signalling and decreased caspase activity. Increased neutrophil survival may have significant consequences in SCD; contributing to leucocytosis, tissue damage and exacerbation of the chronic inflammatory state. [source] The modifying effect of C-reactive protein gene polymorphisms on the association between central obesity and endometrial cancer riskCANCER, Issue 11 2008Wanqing Wen MD Abstract BACKGROUND. Obesity is a major risk factor for endometrial cancer. Obesity, particularly central obesity, is considered as a systemic inflammatory condition and is related strongly to insulin resistance. C-reactive protein (CRP) is the most recognized biologic marker of chronic systematic inflammation, and it is conceivable that the CRP gene may work together with obesity in the development of endometrial cancer. METHODS. On the basis of a population-based case,control study in a Chinese population, the authors obtained obesity measurements and data on 6 CRP single-nucleotide polymorphisms (SNPs) from 1046 patients with newly diagnosed endometrial cancer (cases) and from 1035 age frequency-matched controls. The association of the CRP SNPs with endometrial cancer risk and their modification on the association between obesity and endometrial cancer risk were evaluated. RESULTS. Although CRP SNPs alone were not associated with endometrial cancer, the associations of endometrial cancer with central obesity, measured as the waist-to-hip ratio (WHR) and the waist circumference, seemed to be stronger in women who were homozygous for the major allele of reference SNP (rs)1130864 (cytidine [C]/C) than in women who had the C/thymidine (T) and T/T genotypes (interaction test: P = .013 for WHR; P = .083 for waist circumference). When the women were stratified further by menopausal status, the observed interactions persisted mainly in premenopausal women (interaction test: P < .001 for WHR; P = .002 for waist circumference). CONCLUSIONS. The current results suggested that, in the Chinese population that was studied, obesity-related insulin resistance and proinflammatory effects may play an important role in endometrial cancer risk, and these effects were modified significantly by the CRP SNP rs1130864. Cancer 2008. © 2008 American Cancer Society. [source] Recent developments of dry eye in childrenACTA OPHTHALMOLOGICA, Issue 2009D BREMOND-GIGNAC Purpose Dry eye syndrome in children is a rare disease sometimes difficult to diagnose. The research of the etiology can contribute to adjust the treatment. Methods Two features of dry eye syndrome in children can be distinguished. Dry eye integrated in general disease with evidence of diagnosis and etiology and asymptomatic dry eye which needs a careful check up to recognize the primary etiology. Keratitis sicca usually does not lead to children complaint and simple signs as rubbing or blinking are often observed. Clinical and practical cases are described. Results Review of literature confirms common conditions with adult dry eye but also the specificity of the pediatric dry eye. Dry eye in children is also commonly an inflammatory condition of the ocular surface. New treatment with their indications are listed including tear-like topical therapies and anti-inflammatory or immunosuppressive drugs for ocular surface with specificities in children. Conclusion Dry eye syndrome in children must be recognized and diagnosed. In addition to classical tear-like treatment, specific therapy should be adapted to the etiology. [source] How reliably can autoimmune hypophysitis be diagnosed without pituitary biopsyCLINICAL ENDOCRINOLOGY, Issue 1 2010Trevor A. Howlett Summary Autoimmune hypophysitis is a rare chronic inflammatory condition of the pituitary gland which typically presents with hypopituitarism and a pituitary mass. Cases involving anterior pituitary alone (65%) are six times more common in women, typically presenting during pregnancy or postpartum (57%). Anterior and posterior pituitary involvement (25%) are twice as common in women, and neurohypophysis alone (10%) occurs equally in both sexes. It has a prevalence of around 5 per million, an annual incidence of 1 in 7 to 9 million and in our experience represents the known or suspected cause of 0·5% of cases of hypopituitarism, <1% of pituitary masses and 2% of nonfunctioning macro lesions presenting to an endocrine clinic. However, ,missed' cases of autoimmune hypophysitis may be the aetiology of some other unexplained cases of hypopituitarism. Clinically, headache and visual disturbance are common. Anterior hypopituitarism shows a characteristic but atypical pattern of deficiency of ACTH followed by TSH, gonadotrophins and prolactin deficiency or hyperprolactinaemia. Eighteen percent of cases have evidence of another autoimmune condition. On magnetic resonance imaging (MRI), autoimmune hypophysitis is typically symmetrical and homogeneous with thickened but undisplaced stalk in contrast to typical findings with pituitary tumours. Ultimately, the histological diagnosis of autoimmune hypophysitis can only be confirmed by surgery but a presumptive diagnosis can often be made on the basis of a combination of context and clinical features, and pituitary biopsy is not always clinically necessary for effective clinical management of the patient. [source] Adenocarcinoma in colonic brushing cytology: High-grade dysplasia as a diagnostic pitfallDIAGNOSTIC CYTOPATHOLOGY, Issue 5 2001Gordon H. Yu M.D. Abstract Cytologic evaluation of brushing specimens obtained from the colon may be useful in the diagnosis of neoplastic and inflammatory lesions, as previous studies have reported favorable sensitivity and specificity figures for this procedure. In this study, we report our experience with 80 colonic brushings examined over a 5-yr period. Thirty cases received an atypical or malignant cytologic diagnosis. Nineteen of 20 cases diagnosed cytologically as adenocarcinoma revealed adenocarcinoma on biopsy; one case showed only adenomatous epithelium on biopsy and subsequent resection. Cases diagnosed cytologically as "atypical" or "adenomatous" showed adenocarcinoma, adenoma, and inflammatory conditions upon biopsy. Slides from 30 atypical/malignant cases were retrospectively reviewed for a number of cytomorphologic features and were correlated with the histologic diagnosis. Cases from histologically confirmed adenocarcinoma tended to show greater degrees of altered nuclear polarity, nuclear pleomorphism, membrane irregularities, and chromatin pattern alterations than those from histologically proven adenomatous or inflammatory lesions. The most likely cause of a false-positive diagnosis in this setting is sampling of an adenoma with high-grade dysplasia which fails to meet histologic criteria for adenocarcinoma (invasion of the underlying muscularis mucosae). Thus, in the second part of the study, we examined histologic sections from surgically excised adenomas to determine the frequency with which profound nuclear atypia is at least focally present, potentially resulting in a false-positive cytology diagnosis upon brushing. Slides from 51 cases were reviewed; cytologic atypia beyond that typically observed in adenomas was not observed in 43% of cases. However, profound nuclear atypia was present in 6% of cases; cytologic evaluation of a brushing specimen from these lesions may have resulted in a false-positive diagnosis of adenocarcinoma, despite the histologic diagnosis of adenoma with severe dysplasia. The remaining cases demonstrated intermediate degrees of atypia. These findings serve to quantitate the frequency with which cytohistologic discrepancies might be expected for mass lesions of the colon. Diagn. Cytopathol. 24:364,368, 2001. © 2001 Wiley-Liss, Inc. [source] Salient virulence factors in anaerobic bacteria, with emphasis on their importance in endodontic infectionsENDODONTIC TOPICS, Issue 1 2004Ingar Olsen Endodontic infections by microbial invasion of the necrotic pulp lead to apical periodontitis of both acute and chronic forms. Acute lesions often develop from multiplication of bacteria in primary infections. Such lesions may also occur as exacerbations of chronic forms provoked for example in conjunction with endodontic treatment measures. The clinical course appears related to the character of the microflora. While primary infections are predominated by a mixed flora of anaerobic bacteria and resembles that of aggressive marginal periodontitis, chronic forms of apical periodontitis emerge following regression of the acute infection, whereupon prevailing bacteria have assumed low activity. The significance of virulence factors is easy to understand as far as acute inflammatory conditions are concerned. The role of virulence factors for sustaining chronic inflammation is more unclear and complex. This review is about salient virulence factors in some selected bacterial genera such as Peptostreptococcus, Porphyromonas, Prevotella and Fusobacterium, which often predominate the root canal microbiota in the acute phase of endodontic infections. [source] Nitric oxide and p53 in cancer-prone chronic inflammation and oxyradical overload disease,ENVIRONMENTAL AND MOLECULAR MUTAGENESIS, Issue 1 2004Julie E. Goodman Abstract Nitric oxide (NO·), which is generated under chronic inflammatory conditions that predispose individuals to cancer, has paradoxical effects. NO· can activate p53, which can result in anti-carcinogenic effects, or it can be mutagenic and increase cancer risk. We explored the mechanisms by which NO· induced p53 activation in vitro and found that NO· induced p53 accumulation and phosphorylation, particularly at ser-15, via ATM and ATR kinases, which then led to cell cycle arrest at G2/M. We next examined proteins in these pathways in both inflamed and normal human colon tissue. Inducible nitric oxide synthase (iNOS) levels and p53-P-ser15 levels were positively correlated with the degree of inflammation and with each other. Additionally, the p53 targets, HDM-2 and p21 (WAF1), were present in ulcerative colitis (UC) colon, but undetectable in normal colon, consistent with activated p53. We also found higher p53 mutant frequencies of both G:C , A:T transitions at the CpG site of codon 248 and C:G , T:A transitions at codon 247 in lesional colon tissue from UC cases versus nonlesional tissue from these cases or colon tissue from normal adult controls. Consistent with nitrosative stress and the deamination of 5-methylcytosine, p53 mutations were also detected in sporadic colon cancer tissue and were associated with iNOS activity in these tissues. These studies identified a potential mechanistic link between NO· and p53 in UC and sporadic colon cancer. Environ. Mol. Mutagen. 44:3,9, 2004. Published 2004 Wiley-Liss, Inc. [source] Obesity predisposes to Th17 biasEUROPEAN JOURNAL OF IMMUNOLOGY, Issue 9 2009Shawn Winer Abstract Obesity is associated with numerous inflammatory conditions including atherosclerosis, autoimmune disease and cancer. Although the precise mechanisms are unknown, obesity-associated rises in TNF-,, IL-6 and TGF-, are believed to contribute. Here we demonstrate that obesity selectively promotes an expansion of the Th17 T-cell sublineage, a subset with prominent pro-inflammatory roles. T-cells from diet-induced obese mice expand Th17 cell pools and produce progressively more IL-17 than lean littermates in an IL-6-dependent process. The increased Th17 bias was associated with more pronounced autoimmune disease as confirmed in two disease models, EAE and trinitrobenzene sulfonic acid colitis. In both, diet-induced obese mice developed more severe early disease and histopathology with increased IL-17+ T-cell pools in target tissues. The well-described association of obesity with inflammatory and autoimmune disease is mechanistically linked to a Th17 bias. [source] T-cell-specific deletion of gp130 renders the highly susceptible IL-10-deficient mouse resistant to intestinal nematode infectionEUROPEAN JOURNAL OF IMMUNOLOGY, Issue 8 2009Nicolas Fasnacht Abstract Gp130 is the common receptor of the IL-6 family of cytokines and is involved in many biological processes, including acute phase response, inflammation and immune reactions. To investigate the role of gp130 under inflammatory conditions, T-cell-specific conditional gp130 mice were first bred to the IL-10-deficient background and were then infected with the gastrointestinal nematode Trichuris muris. While IL-10,/, mice were highly susceptible to T. muris, developed a mixed Th1/Th17 response and displayed severe inflammation of the caecum, infection of mice with an additional T-cell-specific deletion of gp130 signalling completely reversed the phenotype. These mice showed an accelerated worm expulsion that was associated with the rapid generation of a strong Th2 immune response and a significant increase in Foxp3-expressing Treg. Therefore, gp130 signalling in T cells regulates a switch between proinflammatory and pathogenic Th1/Th17 cells and regulatory Th2/Treg in vivo. Taken together, the data demonstrate that gp130 signalling in T cells is a positive regulator of inflammatory processes, favouring the Th1/Th17 axis. [source] Intrasplenic trafficking of natural killer cells is redirected by chemokines upon inflammationEUROPEAN JOURNAL OF IMMUNOLOGY, Issue 8 2008Claude Grégoire Abstract The spleen is a major homing site for NK cells. How they traffic to and within this site in homeostatic or inflammatory conditions is, however, mostly unknown. Here we show that NK cells enter the spleen through the marginal sinus and home to the red pulp via a pertussis toxin-insensitive mechanism. Upon inflammation induced by poly(I:C) injection or mouse cytomegalovirus infection, many NK cells left the red pulp while others transiently entered the white pulp, predominantly the T cell area. This migration was dependent on both CXCR3 and CCL5, suggesting a synergy between CXCR3 and CCR5, and followed the path lined by fibroblastic reticular cells. Thus, the entry of NK cells in the white pulp is limited by the expression of pro-inflammatory chemokines. This phenomenon ensures the segregation of NK cells outside of the white pulp and might contribute to the control of immunopathology. [source] Knocking out IL-6 by vaccinationEUROPEAN JOURNAL OF IMMUNOLOGY, Issue 1 2004Pia Galle Abstract Inappropriate expression of IL-6 plays a role in various inflammatory conditions, degenerative diseases, and cancers. Several model systems have been developed that can specifically block IL-6-receptor interactions. Here we present a simple and highly effective approach based on vaccination with a pool of specifically mutated IL-6 analogues to induce a neutralizing IL-6 antibody responsein mice. Judged by the ability of the analogues to bind to heterologous anti-IL-6 antibodies and cellular IL-6 receptors the IL-6 analogues seemed to have a three-dimensional structure comparable to that of wild-type IL-6. Injection of them broke self-tolerance and induced an immune response to IL-6, presumably because of the amino acid differences between the analogues and wild-type IL-6. This resulted in a long-lasting anti-IL-6 antibody-mediated IL-6 deficiency that blocked experimentally induced IL-6-mediated pathology. [source] Mice with neonatally induced inactivation of the vascular cell adhesion molecule-1 fail to control the parasite in Toxoplasma encephalitisEUROPEAN JOURNAL OF IMMUNOLOGY, Issue 5 2003Martina Deckert Abstract Under various inflammatory conditions, cell adhesion molecules are up-regulated in the central nervous system (CNS) and may contribute to the recruitment of leukocytes to the brain. In the present study, the functional role of vascular cell adhesion molecule (VCAM)-1 in Toxoplasma encephalitis (TE) was addressed using VCAMflox/flox MxCre mice. Neonatal inactivation of the VCAM-1 gene resulted in a lack of induction of VCAM-1 on cerebral blood vessel endothelial cells, whereas the constitutive expression of VCAM-1 on choroid plexus epithelial cells and the ependymawas unaffected; in these animals, resistance to T.,gondii was abolished, and VCAMflox/flox MxCre mice died of chronic TE caused by a failure to control parasites in the CNS. Although leukocyte recruitment to the CNS was unimpaired, the B cell response was significantly reduced as evidenced by reduced serum levels of anti- T.,gondii -specific IgM and IgG antibodies. Furthermore, the frequency and activation state of intracerebral T.,gondii -specific T cells were decreased, and microglial activation was markedly reduced. Taken together, these data demonstrate the crucial requirement of VCAM-1-mediated immune reactions for the control of an intracerebral infectious pathogen, whereas other cell adhesion molecules can efficiently compensate for VCAM-1-mediated homing across cerebral blood vessels. [source] CSF analysis in patients with sporadic CJD and other transmissible spongiform encephalopathiesEUROPEAN JOURNAL OF NEUROLOGY, Issue 2 2007A. Green Patients with suspected Creutzfeldt,Jakob disease (CJD) often have routine cerebrospinal fluid (CSF) analysis performed to exclude treatable inflammatory conditions; however, little information is available about the range of results obtained for CSF tests in patients with sporadic CJD and other transmissible spongiform encephalopathies (TSE). Data from 450 patients with sporadic CJD and 47 patients with other TSEs were collected as part of an EC-supported multinational study. Raised white cell counts of >5 cells/,l were found in three of 298 patients with sporadic CJD, with two cell counts of 7 cells/,l and one of 20 cells/,l. Total protein concentrations of >0.9 g/l were found in five of 438 patients with sporadic CJD, although none had a concentration of >1 g/l. CSF oligoclonal IgG was detected in eight of 182 sporadic CJD patients. Of the patients with other TSEs, six had elevated cell counts ranging from 6 to 14 cells/,l but none had total protein concentrations of >0.9 g/l and one patient had detectable oligoclonal IgG. None of the patients with sporadic CJD or other TSEs had abnormalities in all three tests. [source] | ||||||||||||||||||||||||||||||||||||||||