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Activation Products (activation + products)
Selected AbstractsA link between neutrophils and chronic disease manifestations of Chlamydia muridarum urogenital infection of miceFEMS IMMUNOLOGY & MEDICAL MICROBIOLOGY, Issue 1 2010Hyo Y. Lee Abstract Vigorous acute inflammatory responses accompany Chlamydia muridarum infections in mice and are positively correlated with adverse urogenital and respiratory tract infection outcomes in the mouse model. Thus, we tested the hypothesis that neutrophils induce an acute inflammatory insult that, in the repair phase, leads to the chronic sequelae of hydrosalpinx , a surrogate marker of infertility in the mouse model. To this end, we induced neutropenia in mice using a neutrophil-depleting monoclonal antibody during acute phases of C. muridarum urogenital infection only (days 2,21 postinfection). To prove induced neutropenia, peripheral blood was monitored for neutrophils during the treatment regimen. Neutropenic mice had a similar infection course as control mice, but had significantly reduced levels of certain histopathological parameters, reduced production of matrix metalloproteinase-9 (MMP-9) and reduced rates of hydrosalpinx following resolution of the infection. We conclude that neutrophils are a major source of MMP-9, a previously proved pathological factor in this model. Further, we conclude that acute inflammation in the form of neutrophils and neutrophil activation products are at least partially responsible for inducing the histological changes that ultimately result in fibrosis and infertility in the mouse model of chlamydial upper genital tract disease. [source] FEIBA®: mode of actionHAEMOPHILIA, Issue 2004P. L. Turecek Summary., FEIBA®(factor eight inhibitor bypassing activity) has a history of more than 30 years of successful use in controlling bleeding in haemophilic patients who have developed inhibitory antibodies against factor (F)VIII or FIX. Recently it was shown that FEIBA® contains the proenzymes of the prothrombin complex factors, prothrombin, FVII, FIX and FX, but only very small amounts of their activation products, with the exception of FVIIa, which is contained in FEIBA® in greater amounts. FEIBA® controls bleeding by induction and facilitation of thrombin generation, a process for which FV is crucial. A number of biochemical in vitro and in vivo studies have shown that FXa and prothrombin play a critical role in the activity of FEIBA®. Consequently, they are considered to be key components of this product. The prothrombinase complex has been found to be a major target site for FEIBA®. Apart from prothrombin and FXa, FEIBA® contains other proteins of the prothrombin complex, which could also facilitate haemostasis in haemophilia patients with inhibitors. [source] Chylomicron accelerates C3 tick-over by regulating the role of Factor H, leading to overproduction of acylation stimulating proteinJOURNAL OF CLINICAL LABORATORY ANALYSIS, Issue 1 2007Takayuki Fujita Abstract Acylation stimulating protein (ASP) is a fragment of the third component of complement (C3) that is generated in the presence of chylomicron, and plays a role in the synthesis of triacylglycerol by transporting free fatty acids into adipocytes. However, the precise mechanism of ASP generation, especially the role of chylomicron in ASP generation, is unknown. We examined the mechanism through which chylomicron induces ASP generation. Ultracentrifugationally separated chylomicron was incubated with normal human serum (NHS) under various conditions, and the amounts of complement activation products and ASP in the incubation mixture were determined by enzyme-linked immunosorbent assay (ELISA). Upon incubation of NHS with various amounts of chylomicron for 120,min, ASP was generated in a dose-dependent manner. The time course of the production of ASP was similar to the time course of the C3 tick-over phenomenon that occurred by depletion of factor H from the serum. The complement activation induced by chylomicron was different from the usual complement activation that occurs under the regulation of factor H and factor I with respect to the time course and the amount of ASP produced. Our results indicate that chylomicron accelerates C3 tick-over by regulating the role of factor H, leading to the overproduction of ASP. J. Clin. Lab. Anal. 21:14,23, 2007. © 2007 Wiley-Liss, Inc. [source] Anti-Inflammatory Effect of Cardiac Resynchronization TherapyPACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 7 2006KNUT T. LAPPEGÅRD Background: Congestive heart failure (CHF) is associated with persistent immune activation. Medical therapy has been shown to exert only limited anti-inflammatory effects. Cardiac resynchronization therapy (CRT) reduces morbidity and mortality in a subset of patients with heart failure, but it is not known whether this treatment affects the immune system as well. To test this hypothesis, eight patients with heart failure scheduled for CRT were investigated for immune activation before and 6 months after CRT treatment. Methods and Results: After 6 months, all patients had improved in NYHA-class and LVEF, and there was a statistically significant reduction in serum N-terminal pro brain natriuretic peptide (BNP). Furthermore, there was a statistically significant reduction in plasma levels of the chemokines monocyte chemoattractant protein 1 (MCP-1) and interleukin 8 (IL-8) and the cytokine interleukin 6 (IL-6). We observed no changes in the levels of interleukin 1, (IL-1,), tumor necrosis factor , (TNF-,), interleukin 10 (IL-10), or complement activation products. There was a significant correlation between changes in BNP and IL-6 (r = 0.74, P = 0.037). Conclusion: Although based upon a limited number of patients, this report indicates that CRT reduces peripheral markers of immune activation in patients with CHF. Further large scale studies are warranted to verify these findings. [source] Erythrocyte C3d and C4d for monitoring disease activity in systemic lupus erythematosusARTHRITIS & RHEUMATISM, Issue 3 2010Amy H. Kao Objective Disease activity in systemic lupus erythematosus (SLE) is typically monitored by measuring serum C3 and C4. However, these proteins have limited utility as lupus biomarkers, because they are substrates rather than products of complement activation. The aim of this study was to evaluate the utility of measuring the erythrocyte-bound complement activation products, erythrocyte-bound C3d (E-C3d) and E-C4d, compared with that of serum C3 and C4 for monitoring disease activity in patients with SLE. Methods The levels of E-C3d and E-C4d were measured by flow cytometry in 157 patients with SLE, 290 patients with other diseases, and 256 healthy individuals. The patients with SLE were followed up longitudinally. Disease activity was measured at each visit, using the validated Systemic Lupus Activity Measure (SLAM) and the Safety of Estrogens in Lupus Erythematosus: National Assessment (SELENA) version of the Systemic Lupus Erythematosus Disease Activity Index (SLEDAI). Results At baseline, patients with SLE had higher median levels of E-C3d and E-C4d (P < 0.0001) in addition to higher within-patient and between-patient variability in both E-C3d and E-C4d when compared with the 2 non-SLE groups. In a longitudinal analysis of patients with SLE, E-C3d, E-C4d, serum C3, and anti,double-stranded DNA (anti-dsDNA) antibodies were each significantly associated with the SLAM and SELENA,SLEDAI. In a multivariable analysis, E-C4d remained significantly associated with these SLE activity measures after adjusting for serum C3, C4, and anti-dsDNA antibodies; however, E-C3d was associated with the SLAM but not with the SELENA,SLEDAI. Conclusion Determining the levels of the erythrocyte-bound complement activation products, especially E-C4d, is an informative measure of SLE disease activity as compared with assessing serum C4 levels and should be considered for monitoring disease activity in patients with SLE. [source] | ||||||||||