Mouse Anti-Rabbit IgM Hybridoma [OScN]

Fish culture in ponds with heated water offers better fish growth compared to farms in natural sea water temperature, but the increase in temperature favors the development of bacteria and fish disease. In this study, in European sea bass (Dicentrarchus labrax) specimens reared in ponds with heated water from a power plant showing symptoms of a vibriosis-like disease we aimed to characterize the bacterial community as well as some serum metabolic and immune parameters. Bacteriological analysis revealed an important contamination with fecal coliforms, Pseudomonas aeruginosa, Vibrio alginolyticus, yeasts and molds whilst fish tissues from both healthy and diseased specimens were positive for total aerobic flora and several potential pathogenic bacteria such as V. alginolyticus, Aeromonas hydrophila, Pasteurella multocida, P. aeruginosa, Proteus vulgaris and P. mirabilis. Additionally, Grimontia hollisae was only present in diseased fish tissues. Serum metabolic parameters such as aspartate aminotransferase, bile acids, creatine kinase, uric acid, glucose, globulin and potassium were generally increased in diseased fish though only the levels of phosphorous reached a significant level compared to the healthy specimens. Regarding fish innate immunity, our results showed no statistical differences between healthy and diseased fish on peroxidase, protease or antiprotease activity while the bactericidal activity against V. anguillarum was significantly decreased in diseased fish. Lastly, the gene expression of il1b, c3, dic and mpx was down-regulated in the blood of diseased fish while ighm was up-regulated. (C) 2018 PVJ. All rights reserved

Several lines of evidence show that autoimmune responses evolving in type 1 diabetes (T1D) patients include the generation of multi-reactive autoantibody (AutoAb) repertoires, but their role in T1D pathogenesis remains elusive. We tested the hypothesis that variants at the immunoglobulin heavy chain (IGH) locus are genetic determinants of AutoAbs against pancreatic antigens and contribute to T1D susceptibility. With this aim, two independent study designs were used: a case-control study and a family-based cohort comprising a total of 240 T1D patients, 172 first-degree relatives (mother and/or father), and 130 unrelated healthy controls living in Portugal. We found that three SNPs in the IGH locus show suggestive association with T1D with the highest nominal association at rs1950942 (in the IGHM-IGHJ gene region) in both the case-control study (P = 9.35E-03) and the family-based cohort (P = 3.08E-03). These SNPs were also associated with IgG AutoAbs against pancreatic antigens and with AutoAb multi-reactivity in T1D patients. Notably, we found that the SNP with the highest association with T1D susceptibility and IgG autoantibody reactivity (rs1950942) was also associated with anti-GAD IgM reactivity in T1D patients (P = 5.98E-03) and in non-affected parents (P = 4.17E-03). This finding implies that IGH association with autoreactive IgM is detectable irrespective of disease status. These results suggest that genetic variants at the IgM gene region of the IGH locus contribute to antibody autoreactivity and are associated with T1D. We propose that the control of autoantibody generation by IGH polymorphisms is a component of the complex architecture of T1D genetic susceptibility.