The GLI3 may be involved in the damage process of Eimeria tenella to chicken cecal tissue.

Abstract

Eimeria tenella (E. tenella) is the most pathogenic avian coccidial species that targets the cecal epithelial cells of chickens. During the peak period of E. tenella oocyst shedding, the release of a large number of oocysts causes great damage to the cecal tissue. This study uses scanning electron microscopy to observe morphological changes in the host cecum during this period. Subsequently, the metabolic status and transcription level of the cecal tissue were analyzed to gain a comprehensive understanding of the interaction mechanism between E. tenella and the host. The results show substantial cecal tissue damage during the peak oocyst shedding period. The test group shows widespread epithelial cell sloughing, lamina propria exposure, widened intercellular spaces, and a scattered arrangement of absorptive epithelial cells. Combined analysis of the metabolome and transcriptome revealed that primary metabolic pathways, including amino acid metabolism, nucleic acid metabolism and lipid metabolism, were significantly altered in the process of E. tenella damage to cecal tissue. The transcription factor GLI-Kruppel family member 3 (GLI3) may be involved in regulation of primary metabolic pathways through mTORC1 signaling pathway. This study elucidates how E. tenella affects the host through physiological, metabolic and transcriptional changes in chicken cecal tissue. It provides valuable insights into the mechanisms of host immune response and the molecular dynamics of parasite-host interaction.