Microbiota involvement in the pathophysiology of Eimeria tenella infection: focus of the γδ T cells immune response. - Archive ouverte HAL Access content directly
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Microbiota involvement in the pathophysiology of Eimeria tenella infection: focus of the γδ T cells immune response.

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Abstract

Eimeria, an obligatory intracellular parasite, is responsible for coccidiosis and leads to high economic impact in poultry industry. Eimeria tenella (E. tenella) is one of the most pathogenic strains infecting chickens, it colonizes the caecum leading to lesions and to an inflammatory response. A better characterization of the pathophysiology of the infection would provide knowledge that could help modulate the immune response and make it more effective or less deleterious. Neutralization of the pro-inflammatory cytokine IL-17A leads to the decrease in lesions1. Several lymphocytes can produce IL-17A, one of the stronger cell producers being γδ T-cells. To better understand the importance of γδ T-cells in the physiopathology of caecal coccidiosis, we investigated γδ T-cells in the caeca of chickens at homeostasis and during E. tenella infection. The influence of microbiota on this parameter was also investigated. For this purpose, in an original model of conventional and germ-free fast-growing chickens, we studied the evolution of leukocytes and γδ T cells with the infection and analysed the expression of several inflammatory mediators (IFNγ, IL-17A and IL-22) in the caecal tissue and in sorted γδ T cells. Our results showed an increase in the number of leukocytes and γδ T-cells with the infection in conventional chickens. The analysis of different mediators of inflammation in caecal tissues at 7 days post infection showed an increase in mRNAs encoding IFNγ, IL-17A and IL-22 which are cytokines produced in part by γδ T-cells. During the infection, the impact of microbiota on the physiopathology and more particularly on γδ T-cells were studied. Results showed that E. tenella associated-lesions are dependent on the microbiota as well as the IL-17A transcription in caecal tissues. Moreover, administration of microbiota to germ-free chickens at 4 days post-infection restored the caecal lesions and IL-17A transcription to a similar level to conventional chickens. Sorted γδ T-cells from infected animals did not express IL-17A in germ-free compared to conventional chickens. Administration of microbiota restored the gene expression of this cytokine. Altogether, these data suggest that γδ T-cells may contribute to the physiopathology of E. tenella infection. A better characterization of these cells, especially during infection, will allow a better understanding of their contribution to the infection. Furthermore, an immunomodulation of these immune cells may then be able to prevent the negative consequences of the pathology. 1. Del Cacho, E. et al. IL-17A regulates Eimeria tenella schizont maturation and migration in avian coccidiosis. Vet. Res. 45, 25 (2014).
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hal-03824126 , version 1 (21-10-2022)

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  • HAL Id : hal-03824126 , version 1

Cite

Guillaume Sadrin, Laura Sedano, Thierry Chaumeil, Yves Le Vern, Alix Sausset, et al.. Microbiota involvement in the pathophysiology of Eimeria tenella infection: focus of the γδ T cells immune response.. 16. Meeting of the Avian Immunology Research Group (AIRG), Sep 2022, Newark, DE, United States. ⟨hal-03824126⟩
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