Rat Tumor Necrosis Factor alpha

Inflammatory bowel disease (IBD) is a complex immune-mediated disease of gastrointestinal tract that is mainly driven by Th1/Th17 immune response. "Helminth therapy" has emerged, and helminth-derived immunoregulatory molecules are being used as safe and new therapeutic antigens for IBD. Recombinant serine protease (SP) from newborn Trichinella spiralis (T. spiralis) larvae (NBL) was expressed and purified. BALB/c mice were immunized with NBL-SP at 100 mu g three times at an interval of 5 days. Experimental colitis was induced by 2,4,6-trinitrobenzene sulfonic acid (TNBS) administration. The disease activity index (DAI) and macroscopic and microscopic scores of the colon were assessed to identify the effect of NBL-SP on experimental colitis. Cytokine production in the serum was analysed by meso scale discovery (MSD). Cytokine production in the colon was detected by ELISA. CD4(+) T cell differentiation was measured by flow cytometry. NBL-SP alleviated TNBS-induced colitis in mice. The DAI, macroscopic and microscopic scores and colon length all showed a positive intervention effect of NBL-SP on experimental colitis. NBL-SP can weaken the increase in IFN-gamma, TNF-alpha and IL-17 production as well as CD4(+) IFN-gamma(+) T cell and CD4(+) IL-17(+) T cell populations induced by colitis. Furthermore, the levels of Th2-related cytokines (IL-4, IL-5) and regulatory cytokines (IL-10, TGF-beta) were elevated meanwhile the ratio of regulatory T cells (Tregs) and CD4(+) IL-4 T cells were increased by NBL-SP. NBL-SP of T. spiralis had a potential protective effect against IBD. NBL-SP skewed the Th1 and Th17-mediated response towards the Th2 and Treg response.

Abnormality of the immune system may play an important role in the pathogenesis of schizophrenia (SCZ). We aim to investigate the relationship between clinical features of SCZ and tumor necrosis factor-alpha (TNF-alpha) -238 G/A, -308 G/A polymorphisms in SCZ patients by comparing genotype distributions of TNF-alpha gene polymorphisms between patients and healthy controls. A sample of 113 patients with SCZ and 104 healthy volunteers was included in the study. SCID-I was used to confirming the diagnosis according to DSM-IV-TR criteria. We evaluated the patients with some scales and data forms in terms of clinical features, symptom severity, level of insight, suicidal behavior, and treatment response. PCR-RFLP was used to determine TNF-alpha gene polymorphisms from DNA material. The distributions of TNF-alpha - 238 G/A and TNF-alpha - 308 G/A polymorphisms of the patients diagnosed with SCZ were not significantly different from the control group. There was a significant difference in the TNF-alpha - 238 G/A genotype distributions between treatment-resistant and treatment-responsive SCZ patients. Again, the distributions of TNF-alpha - 238 G/A genotype of attempted suicide patients in SCZ were significantly different from the non-attempted suicide of SCZ patients. Whereas TNF-alpha - 238 G/A and -308 G/A polymorphisms were not associated with SCZ, TNF-alpha - 238 G/A polymorphism may be related to treatment resistance and attempted suicide in SCZ patients in the Turkish population.