Regulation of H2S-induced necroptosis and inflammation in broiler bursa of Fabricius by the miR-15b-5p/TGFBR3 axis and the involvement of oxidative stress in this process

Hydrogen sulfide (H2S) is an air pollutant, having toxic effects on immune system. Necroptosis has been discussed as a new form of cell death and plays an important role in inflammation. To investigate the mechanism of H2S-induced immune injury, and the role of microRNAs (miRNAs) in this process, based on the results of high throughput sequencing, we selected the most significantly changed miR-15b-5p for subsequent experiments. We further predicted and determined the targeting relationship between miR-15b-5p and TGFBR3 in HD11 through miRDB, Targetscan and dual-luciferase, and found that miR-15b-5p is highly expressed in H2S-induced necroptosis and inflammation. To understand whether miR-15b-5p/TGFBR3 axis could involve in the process of necroptosis and inflammation, we further revealed that the high expression of miR-15b-5p and the knockdown of TGFBR3 can induce necroptosis. Nec-1 treatment enhanced the survival rate of cells. Notably, H2S exposure induces oxidative stress and activates the TGF-beta pathway, which are collectively regulated by the miR-15b-5p/ TGFBR3 axis. Our present study provides a new perspective for necroptosis regulated by the miR-15b-5p/TGFBR3 axis and reveals a new form of inflammation regulation in immune diseases.

Automated summary

The study investigates the mechanism of immune injury induced by H2S, revealing the important role of miR-15b-5p in necroptosis and inflammation through its targeting relationship with TGFBR3. The research provides a new perspective on the regulation of necroptosis by the miR-15b-5p/TGFBR3 axis and unveils a new form of inflammation regulation in immune diseases.