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

Previous studies demonstrated that Eimeria tenella 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 E. tenella-induced secondary infection by enteropathogenic Escherichia coli (EPEC) was investigated through analyses of host physiological, pathological, and transcriptional changes, as well as cellular structural alterations. Infection with E. tenella 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 INHBA, LEFTY1, IFNG, and ROCK1, indicating host regulatory responses at the genetic level to E. tenella infection that may contribute to elevated TGF-β1 secretion. These findings suggested that E. tenella 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 E. tenella infection and identified potential molecular targets for the development of anti-secondary infection therapeutics.

既往研究表明，柔嫩艾美耳球虫（Eimeria tenella）可引发雏鸡严重的继发性细菌感染，加剧疾病进程并造成更为严重的经济损失。众所周知，转化生长因子-β1（transforming growth factor-β1，TGF-β1）可影响细胞骨架结构，是细菌黏附宿主细胞的关键调控因子。本研究构建了原代鸡胚盲肠上皮细胞（primary chicken embryonic cecal epithelial cell，PCEC）感染模型与鸡体内感染模型，通过分析宿主生理、病理与转录组变化以及细胞结构改变，探究了TGF-β1在柔嫩艾美耳球虫诱导的肠致病性大肠埃希菌（enteropathogenic Escherichia coli，EPEC）继发性感染中的作用。研究发现，柔嫩艾美耳球虫感染可显著提升PCECs的TGF-β1分泌水平，并增强EPEC的黏附能力；外源性给予鸡源TGF-β1可使PCECs发生显著的细胞骨架重构，且经TGF-β1处理后，EPEC的黏附能力呈剂量依赖性升高。盲肠组织转录组分析显示，TGF-β1相关基因（包括INHBA、LEFTY1、IFNG及ROCK1）发生了显著变化，表明宿主在基因层面对柔嫩艾美耳球虫感染产生了调控应答，这可能是TGF-β1分泌升高的原因。上述结果表明，柔嫩艾美耳球虫可通过TGF-β1介导的宿主细胞骨架修饰，促进病原菌黏附。本研究为TGF-β1在柔嫩艾美耳球虫感染过程中促进继发性病原菌感染的作用机制提供了理论依据，并为抗继发性感染治疗药物的开发确定了潜在分子靶点。