{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,28]],"date-time":"2026-09-28T12:01:44Z","timestamp":1790596904164,"version":"4.1.0"},"reference-count":21,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,9,28]],"date-time":"2026-09-28T00:00:00Z","timestamp":1790553600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Immunol."],"abstract":"<jats:sec>\n                    <jats:title>Introduction<\/jats:title>\n                    <jats:p>\n                      <jats:italic>Eimeria tenella<\/jats:italic>\n                      (\n                      <jats:italic>E. tenella<\/jats:italic>\n                      ) preferentially invades the cecum of young chickens and causes enormous economic losses to the global poultry industry.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats: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.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      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 \u00d7 10\n                      <jats:sup>5<\/jats:sup>\n                      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- \u03baB - 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. By contrast, the precocious line specifically activated the PPAR - \u03b3 signaling pathway to negatively restrain excessive inflammation, accompanied by enriched TLR signaling and leukocyte transendothelial migration pathways, thereby forming an immune cascade of \"lipid anti - inflammation - pathogen elimination - mucosal repair\". Immunoprotection trials verified that priming with 1 \u00d7 10\n                      <jats:sup>4<\/jats:sup>\n                      sporulated oocysts of the precocious line significantly alleviated cecal lesions and reduced oocyst output upon secondary challenge, conferring stable mucosal immune protection. The expression trends of seven hub genes (\n                      <jats:italic>PPARG, PLIN1, CYP1A1, THBS1, FMO4, CYP2C18, CXCL14<\/jats:italic>\n                      ) detected via qRT - PCR were consistent with RNA - seq data.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>This study preliminarily elucidated a dual regulatory paradigm consisting of NF - \u03baB - mediated tissue injury and PPAR - \u03b3 - dependent anti - inflammatory responses, refined the mucosal immune theoretical framework for commercially available precocious attenuated strains, and provided candidate molecular targets for targeted anti - coccidial intervention in chickens.<\/jats:p>\n                  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