Physiopathology of Eimeria tenella infection and integrity of the intestinal barrier: influence of the microbiota
Résumé
Eimeria tenella infection results in a severe intestinal disease leading to high economic impact in poultry industry. Coccidiosis is frequently associated with a high prevalence of opportunistic infections. Our objective was to study the importance of the microbiota on the physiopathology of the infection. Using an original model of germ-free and conventional broilers, our results show that, at a similar parasite load, lesions caused by E. tenella are dependent on the microbiota. At seven days post-infection, an increase of some inflammatory mediators is detected in the caecal tissue both in conventional and germ-free chickens whereas other inflammatory mediators are expressed only in a microbiota-dependent manner. Del Cacho et al 2014 showed that the neutralization of IL17A led to less lesions. In our study, IL-17A is increased only in conventional infected chickens. Administration of a conventional microbiota to germ-free chickens 4 days after infection restored caecal lesions and the expression of IL-17A. Among inflammatory cells producing IL-17A, we showed that T cells were the major producers suggesting that these cells may play a role in the physiopathology of this infection. Lesions represent a rupture of the intestinal barrier, which, at homeostasis, protects against invasion of commensal bacteria. Using a non-pathogenic E. coli strain administered by oral route, we confirmed a dissemination in the spleen during E. tenella infection. In conclusion, in E. tenella infection, the microbiota facilitates with a strong inflammatory response and the alteration of the intestinal barrier leading to bacterial translocation responsible for opportunistic infections.