Mouse TNF-α(Tumor Necrosis Factor Alpha) ELISA Kit

Nitrite can cause fishes poisoning. This study evaluated the effects of nitrite exposure on haematological status, ion concentration, antioxidant enzyme activity, immune response, cytokine release and apoptosis in yellow catfish. In this study, yellow catfish were exposed to three levels of nitrite (0, 3.00 and 30.00 mg L-1) for 96 h. The results showed that nitrite poisoning could lead to blood deterioration (red blood cell and hemoglobin reduced; white blood cell and methemoglobin elevated), ion imbalance (Na+ and Cl- declined; K+ elevated), oxidative stress (total antioxidant capacity, superoxide dismutase, catalase and glutathione peroxidase activities declined; malondialdehyde accumulation), immunosuppression (lysozyme activity, 50% hemolytic complement, immunoglobulin M, respiratory burst and phagocytic index declined) and cytokines release (TNF, IL 1 and IL 8 elevated). In addition, nitrite poisoning could induce up-regulation of antioxidant enzymes (Cu/Zn-SOD, Mn-SOD, CAT and GPx), cytokines (TNF, IL 1 and IL 8) and apoptosis (P53, Bax, Cytochrome c, Caspase 3, Caspase 9, ERK and JNK) genes transcription. This study suggesting that the nitrite exposure triggers blood deterioration, disrupts the ionic homeostasis, induces oxidative stress, immunosuppression, inflammation and apoptosis in yellow catfish.

Background: Pregnancy-specific beta 1-glycoproteins are capable of regulating innate and adaptive immunity, exerting predominantly suppressive effects. In this regard, they are of interest in terms of their pharmacological potential for the treatment of autoimmune diseases and post-transplant complications. The effect of these proteins on the main pro-inflammatory subpopulation of T lymphocytes, IL-17-producing helper T cells (Th17), has not been comprehensively studied. Therefore, the effects of the native pregnancy-specific beta 1-glycoprotein on the proliferation, Th17 polarization and cytokine profile of human CD4(+) cells were assessed. Results: Native human pregnancy-specific beta 1-glycoprotein (PSG) at a concentration of 100 mu g/mL was shown to decrease the frequency of Th17 (ROR gamma tau(+)) in CD4(+) cell culture and to suppress the proliferation of these cells (ROR gamma tau(+)Ki-67(+)), along with the proliferation of other cells (Ki-67(+)) (n = 11). A PSG concentration of 10 mu g/mL showed similar effect, decreasing the frequency of Ki-67(+) and ROR gamma tau(+)Ki67(+) cells. Using Luminex xMAP technology, it was shown that PSG decreased IL-4, IL-5, IL-8, IL-12, IL-13, IL-17, MIP-1 beta, IL-10, IFN-gamma, TNF-alpha, G-CSF, and GM-CSF concentrations in Th17-polarized CD4(+) cell cultures but did not affect IL-2, IL-7, and MCP-1 output. Conclusions: In the experimental model used, PSG had a mainly suppressive effect on the Th17 polarization and cytokine profile of Th17-polarized CD4(+) cell cultures. As Th17 activity and a pro-inflammatory cytokine background are unfavorable during pregnancy, the observed PSG effects may play a fetoprotective role in vivo.