Impact of heat stress on intestinal histopathology and cellular immune response in chickens infected with Eimeria tenella.

Abstract

This study was conducted to investigate the pathological characteristics and cellular immune response of chickens infected with Eimeria tenella under heat stress conditions. A total of 140 chicks were randomly assigned to four groups: a control group (CON), a group infected with E. tenella (Et), a heat stress group (HS), and a heat stress group infected with E. tenella (HS-Et). The HS and HS-Et groups were maintained at 38&#xa0;&#xb1;&#xa0;1&#xa0;&#xb0;C from 1 to 24&#xa0;days old, while chickens in the CON and Et group were raised in thermoneutral conditions. At 14&#xa0;days old, chicks in the Et and HS-Et groups were orally inoculated with 2&#xa0;&#xd7;&#xa0;10sporulated E. tenella oocysts. Fecal samples were collected between 4 and 10&#xa0;days post-inoculation (dpi) to quantify oocyst shedding. Chickens were sacrificed at 0, 5, and 10 dpi for histopathological examination and cytokines gene (IL-12, IL-1&#x3b2;, IFN-&#x3b3;, IL-4, IL-10, IL-13) expression analysis using qRT-PCR. The results showed that although fecal oocyst shedding was significantly lower in the HS-Et group compared to the Et group (P&#xa0;<&#xa0;0.05), the histopathological lesion scores were highest in this group at 10 dpi. There were no significant differences in Th1 and Th2 cytokines expression levels among the three infected groups, except for IL-12. Notably, IL-12 expression was significantly higher in the HS-Et group than in the other three groups. These findings suggest that heat stress suppresses the growth of E. tenella but exacerbates tissue damage by enhancing inflammation and activating the Th1 response via the IL-12 pathway.