raw data-Eimeria tenella can promote secondary EPEC infection in hosts by increasing the chicken TGF-β1.zip

Previous studies demonstrated that <i>Eimeria tenella</i> induced severe secondary bacterial infections in chicks, exacerbating disease progression and causing greater economic losses. It was well known that transforming growth factor-β1 (TGF-β1) influenced cytoskeletal architecture, serving as a key factor for bacterial adhesion to host cells. In this study, both a primary chicken embryonic cecal epithelial cell (PCEC) infection model and an in vivo chicken infection model were established. The role of TGF-β1 in <i>E. tenella</i>-induced secondary infection by enteropathogenic <i>Escherichia coli</i> (EPEC) was investigated through analyses of host physiological, pathological, and transcriptional changes, as well as cellular structural alterations. Infection with <i>E. tenella</i> significantly enhanced TGF-β1 secretion by PCECs and increased EPEC adhesion. Exogenous administration of chicken TGF-β1 led to pronounced cytoskeletal remodeling in PCECs, and EPEC adhesion was dose-dependently increased following TGF-β1 treatment. Transcriptomic analysis of cecal tissue revealed significant changes in TGF-β1–associated genes, including <i>INHBA</i>, <i>LEFTY1</i>, <i>IFNG</i>, and <i>ROCK1</i>, indicating host regulatory responses at the genetic level to <i>E. tenella</i> infection that may contribute to elevated TGF-β1 secretion. These findings suggested that <i>E. tenella</i> promoted pathogenic adhesion via TGF-β1–mediated cytoskeletal modifications in host cells. The study provided a mechanistic basis for the role of TGF-β1 in facilitating secondary pathogen infections during <i>E. tenella</i> infection and identified potential molecular targets for the development of anti-secondary infection therapeutics.