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Circulating Neutrophils (circulating + neutrophil)
Selected AbstractsPathophysiologic 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] The main neutrophil and neutrophil-related functions may compensate for each other following exercise,a finding from training in university judoistsLUMINESCENCE: THE JOURNAL OF BIOLOGICAL AND CHEMICAL LUMINESCENCE, Issue 1 2007Noriko Mochida Abstract In order to clarify the relationship between exercise and neutrophil function, we measured three major neutrophil and neutrophil-related functions, viz. the reactive oxygen species (ROS) production capability and phagocytic activity (PA) of neutrophils and serum opsonic activity (SOA), simultaneously before and after a unified loading exercise under three different sets of conditions. Thirteen female collegiate judoists were examined with a unified exercise loading (2 h) immediately before and after a 64 day training period. Immediately thereafter, the athletes took part in a 6 day intensified training camp, following which the same exercise loading was repeated. Responses from circulating neutrophils were estimated by comparing the two sets of values obtained before and after the two instances of exercise loading. The parameters assessed included neutrophil count, SOA, PA and ROS production capability. ROS production increased after the exercise loading performed immediately before and after the 64 day training period just before the camp, (p < 0.01) but decreased following the exercise loading performed after the camp (p < 0.05). This suggested depressed bacteriocidal capability of the circulating neutrophils. PA decreased after the exercise loading sessions imposed prior to and after the 64 day training period (p < 0.01) but did not change in the loading session after the camp. No changes were seen in SOA produced with the loading exercise either before the 64 day exercise period or before the camp, but increased significantly following the post-camp session (p < 0.05). In conclusion, athletic training-induced changes in immune functional activities of neutrophils, such as ROS production and PA, and neutrophil-related factors, such as SOA, may compensate for each other to maintain the overall integrity of the neutrophil immune function. Copyright © 2006 John Wiley & Sons, Ltd. [source] Neutropenia in the acute phase of Kawasaki disease and prevention of coronary artery aneurysmPEDIATRICS INTERNATIONAL, Issue 4 2009Zenshiro Onouchi Abstract Background:, The significance of neutropenia in Kawasaki disease (KD) has not been fully elucidated as yet. Methods:, Subjects were retrospectively sampled from two clinical trials. These patients treated with aspirin alone (ASA) and PolyglobinN-Bayel (PolyN) given as i.v. immunoglobulin were categorized as ASA-early (n = 0), ASA-late (n = 8), PolyN-early (n = 18), or PolyN-late (n = 27) based on the therapy administered and the incidence of neutropenia before the 10th day of illness (DI) and after 11 DI. Data regarding the time of onset of neutropenia, and incidence of coronary artery lesion (CAL) formation were obtained. P < 0.05 was considered statistically significant. Results:, No patients in the ASA group exhibited neutropenia within 10 DI. The time of onset of neutropenia in the PolyN-early group was 8 ± 1.3 DI. That in the PolyN-late group (19.8 ± 8 DI) was earlier than in the ASA-late group (26.6 ± 14 DI; P < 0.025). PolyN-early patients had a lower incidence of CAL formation than ASA-non patients (patients without neutropenia in the ASA group; P = 0.00019) and ASA-late patients (P = 0.04). That in the PolyN-early group tended to be lower than in the PolyN-late group (P < 0.1). Conclusion:, Early neutropenia indicated that circulating neutrophils within 10 DI may play an indispensable role in the following sequence to CAL formation in KD. [source] Coexpression of CD177 and membrane proteinase 3 on neutrophils in antineutrophil cytoplasmic autoantibody,associated systemic vasculitis: Anti,proteinase 3,mediated neutrophil activation is independent of the role of CD177-expressing neutrophilsARTHRITIS & RHEUMATISM, Issue 5 2009N. Hu Objective Wegener's granulomatosis (WG) is strongly associated with antineutrophil cytoplasmic autoantibodies (ANCAs) directed against proteinase 3 (PR3). Recent studies have shown that membrane-bound PR3 (mPR3) is differentially expressed and colocalizes with CD177/NB1 on circulating neutrophils. We undertook this study to assess the differential expression of CD177 on neutrophils from patients with ANCA-associated systemic vasculitis (ASV) in comparison with patients with systemic lupus erythematosus (SLE), patients with rheumatoid arthritis (RA), and healthy individuals, and to investigate whether colocalization of mPR3 and CD177 affects anti-PR3,mediated neutrophil activation. Methods Expression of CD177 and mPR3 was analyzed by flow cytometry on isolated neutrophils from patients with ASV (n = 53), those with SLE (n = 30), those with RA (n = 26), and healthy controls (n = 31). Neutrophil activation mediated by anti-PR3 antibodies was assessed by measuring the oxidative burst with a dihydrorhodamine assay. Results Percentages of CD177-expressing neutrophils were significantly higher in patients with ASV and those with SLE than in healthy controls. In 3 healthy donors, CD177 expression was not detected. After priming with tumor necrosis factor ,, neutrophils remained negative for CD177 while mPR3 expression was induced. Neutrophils from CD177-negative donors or CD177, neutrophils sorted from donors with bimodal expression were susceptible to anti-PR3,mediated oxidative burst. Variation in the extent of anti-PR3,mediated neutrophil activation among different donors occurred independent of the percentage of CD177-expressing neutrophils. Conclusion Membrane expression of CD177 on circulating neutrophils is increased in patients with ASV and in those with SLE, but not in RA patients. However, primed neutrophils from CD177-negative individuals also express mPR3 and are susceptible to anti-PR3,mediated oxidative burst, suggesting that recruitment of CD177-independent mPR3 is involved in anti-PR3,induced neutrophil activation. [source] Improving the outcome of cord blood transplantation: use of mobilized HSC and other cells from third party donorsBRITISH JOURNAL OF HAEMATOLOGY, Issue 2 2009Manuel N. Fernández Summary We developed the strategy of umbilical cord blood transplants (UCBT) with co-infusion of a limited number of highly purified mobilized haematopoietic stem cells (MHSC) from a human leucocyte antigen (HLA) unrestricted third party donor (TPD). Short post-transplant periods of neutropenia were usually observed in adults with haematological neoplasms receiving UCBT with a relatively low cell content and 0,3 HLA mismatches after myeloablative conditioning. This resulted from an early and initially predominant engraftment of the TPD,MHSC. After a variable period of double complete TPD + UCB chimerism, final full UCB chimerism was achieved (cumulative incidence >90%) within 100 d. Early recovery of the circulating neutrophils resulting from the ,bridge transplant' of the TPD,MHSC reduced the incidence of serious neutropenia-related infections, also facilitating the use of drugs with myelosuppressive side effects to combat other infections. The observed incidence of graft- versus -host disease and relapses was low, with overall and disease-free survival curves comparable to those of HLA identical sibling transplants. Post-transplant recovery of natural killer cells occurred soon after the transplant and B cells recovered around 6 months, but T-cell recovery took more than 1 year. Available data show that T cell recovery derives from UCB,HSC through thymic differentiation and that cytomegalovirus (CMV)-specific lymphocytes develop following CMV reactivations. [source] | ||||||||||