Abstract
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-κB, 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.
Highlights
Avian coccidiosis caused by the intracellular protozoan Eimeria is responsible for severe economic losses in the global poultry industry [1, 2]
The protein expression levels of chicken Toll-like receptor 15 (ChTLR15) and chicken NOD-like receptor 3 (NLRP3) (ChNLRP3) (Figure 2B) and Chicken interleukin 1 Beta (ChIL-1β) (Figure 2C) in the ceca of Eimeria-infected chickens exhibited similar dynamic changes at 4, 12, 24 and 72 h pi. These results indicated that both the ChTLR15/Chicken nuclear transcription factor-κB (ChNF-κB) and ChNLRP3/ChIL-1β pathways were activated in the sporozoite stage during E. tenella infection
While we focused on the roles of Toll-like receptors (TLRs) during Eimeria infection, we are interested in ChTLR15
Summary
Avian coccidiosis caused by the intracellular protozoan Eimeria is responsible for severe economic losses in the global poultry industry [1, 2]. Eimeria tenella is one of the most pathogenic species because it invades chicken cecum epithelial cells and causes severe pathological lesions in the ceca. Long-term measures against coccidiosis have gradually shown unavoidable drawbacks, including residues of chemical drugs in poultry meat, emergence of Eimeria strains with drug resistance, and pathogenic reversion of live parasite vaccines [3, 4]. A deep understanding of the mechanism of parasite invasion into host cells is a prerequisite for developing novel vaccines or drugs. The invasion mechanism of Eimeria parasites is not clear, the activation of related signal transduction pathways during Eimeria invasion into host cells plays a vital role [5–7].
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