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Abstract
Host responses to parasitic infections are complex and involve many facets of cellular and humoral immune mechanisms. Many intestinal infections in poultry, such as coccidiosis represent economically important diseases for the poultry industry. Coccidiosis is caused by intracellular protozoan parasites belonging to several different species of the genus Eimeria and cause of impaired the growth, higher feed conversion and mortality in poultry. Heat stress (HS) is one of the major environmental stresses in the poultry industry and results in direct losses to production. HS results in reduced oocyst output in chickens. The general objective of this work is to understand the interplay between HS and Eimeria spp. pathogenesis in meat-type chickens. We herein provide new perspectives for studies with coccidiosis in poultry, combining stablished knowledge with molecular biology to provide a bigger overview of the pathogenicity of the infection with focus on heat stress of the host. The results of this work demonstrate that heat stress significantly reduces development of asexual stages of E. tenella. We also show that the reduced outcome of E. maxima infection in poultry is result of the reduced sexual reproduction of this parasite in the intestine, and that infection with E. maxima leads to disruption of the intestinal barrier by differential regulation of tight junction genes, resulting in increased intestinal permeability and cellular influx. Lastly, our results indicate a second peak of replication of E. maxima without reinfection, not previously reported in the literature. Understanding the nature of the diminished outcome of infection in heat stressed chickens provides basis for future research seeking new methods of preventing and controlling the disease.