Jianqiang Tang, Meihui Tang, Liyue Dong, Areej Arif, Jin Zhang, Tao Zhang, Genxi Zhang, Kaizhou Xie, Zhenhua Zhao, Guojun Dai
Avian coccidiosis, caused by several species of the genus Eimeria, remains a major constraint on poultry production, with Eimeria tenella (E. tenella) representing an important pathogenic species that primarily infects the chicken cecum. Host genes associated with the inflammatory response may provide useful candidates for resistance evaluation. In our previous transcriptome analysis, serum and glucocorticoid-induced kinase 1 (SGK1), fatty acid binding protein 1 (FABP1), and bone morphogenetic protein 3 (BMP3) were identified as candidate genes in yellow-feathered broilers. Here, these genes were re-evaluated by RT-qPCR in a commercial Jinghai Yellow chicken population after E. tenella infection, followed by correlation analysis with inflammatory cytokine expression and further in vitro functional analysis of SGK1. Cecal tissues from infected birds showed increased expression of IL-6, CXCLi2, TNF-α, SGK1, FABP1, and BMP3, whereas IL-10 was decreased. Among the 3 candidate genes, SGK1 showed the most consistent associations with inflammatory mediators in both control and infected birds, displaying positive correlations with IL-6, CXCLi2, and TNF-α and a negative correlation with IL-10. In DF-1 and HD11 cells, SGK1 overexpression reduced pro-inflammatory cytokine expression and secretion and increased IL-10, whereas SGK1 knockdown produced the opposite pattern under basal and sporozoite-stimulated conditions. Flow-cytometric analysis further showed that SGK1 manipulation affected the proportion of fluorescent sporozoite-positive cells and the apoptotic response induced by sporozoite exposure. These findings suggest that SGK1 is associated with the early cecal inflammatory response to E. tenella and may modulate early host-cell responses, including cytokine expression, sporozoite-positive cell proportion, and apoptosis, in chicken-derived cell models. Therefore, SGK1 represents a promising candidate for further investigation in host-response studies of E. tenella, although the downstream signaling pathways and intracellular parasite-development processes involved remain to be defined.