Host responses to Clostridium perfringens challenge in a chicken model of chronic stress

This study utilized a chicken model of chronic physiological stress mediated by corticosterone (CORT) administration to ascertain how various host metrics are altered upon challenge with . Necrotic enteritis (NE) is a disease of the small intestine of chickens incited by , which can result in elevated morbidity and mortality. The objective of the current study was to investigate how physiological stress alters host responses and predisposes birds to subclinical NE. Birds administered CORT exhibited higher densities of in their intestine, and this corresponded to altered production of intestinal mucus. Characterization of mucus showed that treatment altered the relative abundance of five glycans. Birds inoculated with did not exhibit evidence of acute morbidity. However, histopathologic changes were observed in the small intestine of infected birds. Birds administered CORT showed altered gene expression of tight junction proteins (i.e. and ) and toll-like receptors (i.e. and ) in the small intestine. Moreover, birds administered CORT exhibited increased expression of and - in the spleen, and , , , , and in the thymus. Body weight gain was impaired only in birds that were administered CORT and challenged with . CORT administration modulated a number of host functions, which corresponded to increased densities of in the small intestine and weight gain impairment in chickens. Importantly, results implicate physiological stress as an important predisposing factor to NE, which emphasizes the importance of managing stress to optimize chicken health.