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Avian coccidiosis caused by  Eimeria  leads to severe economic losses in the global poultry industry. Although chicken Toll-like receptor 15 (ChTLR15) was reported to be involved in  Eimeria  infection, the detailed mechanism underlying its role in the inflammatory response remains to be discovered. The present study demonstrated that the mRNA expression levels of ChTLR15, ChMyD88, ChNF- κ B, ChNLRP3, ChCaspase-1, ChIL-18 and ChIL-1β and the protein levels of ChTLR15 and ChNLRP3 in cecal tissues of  Eimeria -infected chickens were significantly elevated at 4, 12, and 24 h compared with those in noninfected control chickens ( p  < 0.01). Moreover, the mRNA levels of molecules in the ChTLR15/ChNF-κB and ChNLRP3/ChIL-1β pathways and the protein levels of ChTLR15 and ChNLRP3 in chicken embryo fibroblast cells (DF-1) stimulated by  E. tenella  sporozoites were consistent with those in  Eimeria -infected chickens. Furthermore, overexpression of ChTLR15 in DF1 cells augmented activation of the ChTLR15/ChNF-κB and ChNLRP3/ChIL-1β pathways when stimulated with  E. tenella  sporozoites, while knockdown of ChTLR15 in DF1 cells showed inverse effects. Taken together, the present study provides evidence that  E. tenella  sporozoites specifically activate ChTLR15 and then trigger activation of the ChNLRP3/ChIL-1β pathway, which partially mediates inflammatory responses to  Eimeria  infection.

Activation of ChTLR15/ChNF-κB-ChNLRP3/ChIL-1β signaling transduction pathway mediated inflammatory responses to E. tenella infection