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Abstract
Meat-type (broiler) chickens are fast-growing and possess a highly efficient gastrointestinal tract making them vulnerable to multiple infections and stressors. Coccidiosis is an intestinal parasitic disease induced by Eimeria spp infection causing feed intake and growth reduction, high morbidity, and mortality leading to severe economic losses. An uncontrollable coccidiosis outbreak frequently exists due to the parasite's mutation capacity to develop drug resistance. Eimeria (E.) maxima is a highly pathogenic species that infects the middle jejunum and ileum, disrupting and damaging the intestinal mucosal lining, and predisposing the midgut for secondary infection. Heat stress (HS) is the most prevalent environmental stressor that ubiquitously affects broiler chicken houses. Heat stress negatively impacts feed intake and conversion, growth, and increases the mortality rate resulting in severe losses. The combination of two stressors, HS and Eimeria spp infection, is a common condition in the poultry field. Previous research reported that exposing Eimeria spp-infected chickens to HS suppressed parasitic shedding. We, therefore, utilized the model of infecting broiler chickens with E. maxima under either thermoneutral or HS condition to delineate the ileum response to each individual stressor and their combination aiming to elucidate the mechanism by which HS curtail Eimeria spp life cycle. The research outcomes showed that exposing E. maxima-infected chickens to HS mitigated the parasite’s pathogenic effect on ileum function, digestibility, and nutrient transporters, and prevented the villus/crypt atrophy and inducible oxidative damage caused by E. maxima. The transcriptome analysis of ileum tissue expectedly demonstrated the enrichment of the immune functions in response to E. maxima infection. The downregulation of immune pathways and protein synthesis and upregulation of amino acids and lipid metabolism were observed in response to HS. Combining HS and E. maxima altered the cellular and molecular responses associated with each stressor when solely applied. Interestingly the nutrient metabolism and calcium signaling were uniquely altered in E. maxima-infected chickens compared to the other groups exposed either to infection or heat treatment. This suggests that limiting the nutrients available to be acquired by E. maxima may be the mechanism by which HS limits the parasite's pathogenicity.