This study aims to investigate effects of polymorphisms in key Th-17 immune response genes on the susceptibility to HBeAg-positive (HBeAg) chronic hepatitis B (CHB) and response to PEG-IFNa-2α. A total of 139 patients with HBeAg CHB treated with PEG-IFNa-2α and 145 healthy controls were enrolled to explore the association between IL-17A, IL-17F, IL-21 and IL-23R polymorphisms and HBeAg CHB susceptibility, as well as treatment efficacies. Genotypes were determined by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) and DNA sequencing. IL-17A rs4711998 and IL-17F rs763780 may affect susceptibility to HBeAg CHB and response to PEG-IFNa-2α treatment. The T allele of IL-21 rs12508721 may lower HBeAg CHB susceptibility but enhance PEG-IFNa-2α response, and the GA genotype and the A allele of IL-23R rs11209026 may reduce the susceptibility to HBeAg CHB. Th17-related gene polymorphisms were linked to HBeAg CHB susceptibility, and rs4711998, rs763780 and rs12508721 were associated with sustained responses to PEG-IFNa-2α.

This study investigated the alleviating effects of hydrogen sulfide (H2S), derived from sodium hydrosulfide (NaHS), on inflammation induced by dextran sulfate sodium (DSS) in both in vivo and in vitro models. We found that NaHS injection markedly decreased rectal bleeding, diarrhea, and histological injury in DSS-challenged mice. NaHS (20 μmol/L) reversed DSS-induced inhibition in cell viability in Caco-2 cells and alleviated pro-inflammation cytokine expression in vivo and in vitro, indicating an anti-inflammatory function for H2S. It was also found that H2S may regulate cytokine expression by inhibiting the nuclear factor-κB (NF-κB) signaling pathway. In conclusion, our results demonstrated that H2S alleviated DSS-induced inflammation in vivo and in vitro and that the signal mechanism might be associated with the NF-κB signaling pathway.