Supplementary file 2_Transcriptomic analysis of cecal mucosal immunity in SPF White Leghorn chicks infected with precocious and parent strains of Eimeria tenella.xls

Introduction<p>Eimeria tenella (E. tenella) preferentially invades the cecum of young chickens and causes enormous economic losses to the global poultry industry.</p>Methods<p>In this study, we established chicken infection models for the virulent parent strain and its precocious attenuated line, and collected samples at 2 dpi and 6 dpi as two critical time points. By integrating pathogenicity evaluation, transcriptome sequencing, detection of mucosal immune-related indicators, and homologous challenge protection assays, we systematically revealed the distinct molecular mechanisms underlying strain-specific differences in pathogenicity and immune regulation.</p>Results<p>Pathogenicity results showed that increased infection dosages suppressed weight gain and aggravated bloody diarrhea and oocyst shedding in both strains.

In particular, infection with 1 × 10⁵ sporulated oocysts of the parent strain caused massive chick mortality, while the precocious line exhibited markedly lower virulence. Transcriptomic data revealed that gametogony (6 dpi) represented the peak of host immune response. The parent strain persistently overactivated the NF- κB - mediated positive feedback cascade of coagulation and complement as well as ECM remodeling, triggering steroid metabolic disorder and antioxidant exhaustion, which ultimately induced severe hemorrhagic necrosis of the cecum.