TRAF6, a gga-miR-7b Target, Promotes Eimeria tenella-Induced Inflammation and Apoptosis in Chickens by Activating NF-κB Pathway.

Chicken coccidiosis, a severe intestinal parasitic disease caused by Eimeria protozoa, causes substantial annual economic losses to the global poultry industry. This study focused on investigating the role of tumor necrosis factor receptor (TNFR)-associated factor 6 (TRAF6) in modulating chicken innate immune responses against Eimeria tenella (E. tenella) infections. Here, we show that TRAF6 is sensitive to the process of E. tenella infection, and cecal tissue responds to the early infection of E. tenella by up-regulating the expression of TRAF6. Specifically, TRAF6 overexpression enhances E. tenella-induced activation of the NF-κB pathway (a core innate immune signaling cascade), thereby promoting host inflammatory cytokines production and cell apoptosis, while TRAF6 knockdown mitigates these pathological effects. Mechanistically, TRAF6-mediated regulation of NF-κB pathway activation and inflammatory responses during E. tenella infection can be specifically targeted by key microRNAs (miRNA), gga-miR-7b, in chickens. Taken together, this study identifies that TRAF6 plays an important regulatory role in innate immune response against E. tenella infection, providing novel insights into host-parasite interactions and potential targets for coccidiosis control.