Physiopathology of Eimeria tenella infection and integrity of the intestinal barrier: influence of the microbiota
Résumé
Eimeria tenella infection leads to 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 during E. tenella infection the importance of immune cells and mediators of the inflammatory response on the severity of caecal lesions and on the potential dissemination of commensal bacteria. An original model of germ-free and conventional broilers chickens was developed to study the impact of the caecal microbiota on the physiopathology of the infection. Our results show that, at the same parasite load, lesions caused by E. tenella are dependent on the microbiota. Seven days post-infection, an increase of inflammatory mediators (interferon-g, colony stimulating factor, CSF-1, 2) are detected at the caecal tissue level in conventional chickens and germ-free chickens whereas interleukin-17A (IL-17A) is increased only in conventional chickens. Moreover, administration of microbiota to germ-free chickens 4 days post-E. tenella infection restored the caecal lesions and the expression of IL-17A to a similar level to conventional chickens suggesting that inflammatory cells producing IL-17A could play a role in the physiopathology of the infection. The lesions represent a rupture of the intestinal barrier, which, at homeostasis, protects the chicken against invasion of commensal bacteria. Our hypothesis is that intestinal lesions caused by the infection would lead to commensal bacterial translocation. This was confirmed with a non-pathogenic E. coli strain administered by oral route that presented a dissemination in the spleen during E. tenella infection. In conclusion, during infection, the microbiota is responsible for the inflammatory response via IL-17A and the formation of lesions. The loss of the intestinal integrity leads to commensal bacterial translocation that could contribute to the development of opportunistic diseases.