Background <p>Chicken coccidiosis caused by <i>Eimeria tenella</i> (<i>E</i>. <i>tenella</i>) poses a major threat to global poultry production, with its tropism for the caecal microenvironment and dynamic interactions with the resident microbiota remaining incompletely understood. The caecal microbiota plays a critical role in host‒parasite interplay, yet the mechanisms through which microbial homeostasis influences <i>E</i>. <i>tenella</i> development and host resistance remain elusive. This study aimed to elucidate the causal relationship between caecal dysbiosis and <i>E</i>. <i>tenella</i> pathogenesis, with a focus on identifying microbiota-derived regulators of parasite development and host immunity.</p> Results <p>Antibiotic-induced caecal dysbiosis (ABX) significantly impaired <i>E</i>. <i>tenella</i> macrogametogenesis, demonstrating microbiota-dependent regulation of parasitic development. Faecal microbiota transplantation (FMT) validated this causal link, revealing that microbial reconstitution restored parasite maturation. Notably, <i>Intestinimonas</i> spp. were identified as key inhibitors of <i>E</i>. <i>tenella</i> development through transcriptional regulation of the <i>EtGFAT</i> gene (<i>Eimeria tenella</i> glucosamine: fructose-6-phosphate aminotransferase), a critical mediator of macrogamete formation. Furthermore, the transplantation of <i>Intestinimonas butyriciproducens</i> (<i>I</i>. <i>butyriciproducens</i>) attenuated clinical manifestations of infection while increasing IFN-γ secretion from CD8<sup>+</sup> T lymphocytes, thereby enhancing host resistance to <i>E</i>. <i>tenella.</i></p> Conclusions <p>This study revealed that caecal microbiota homeostasis is indispensable for <i>E</i>. <i>tenella</i> developmental progression and highlights <i>Intestinimonas</i> as a pivotal microbial regulator of parasite biology. The dual role of <i>I</i>. <i>butyriciproducens</i> in suppressing parasitic virulence and potentiating adaptive immune responses underscores the therapeutic potential of microbiota-targeted strategies. These findings provide a foundation for the development of novel anticoccidial interventions through targeted manipulation of caecal microbial communities.</p> <p><MediaObject ID="MOESM2"> <VideoObject FileRef="MediaObjects/40168_2025_2302_MOESM2_ESM.mp4" VideoID="5Cy5Mc4VAP6nJweNtMmFML"> <Caption Language="En" xml:lang="en"> <CaptionContent> <p>Video Abstract</p> </CaptionContent> </Caption> </VideoObject> </MediaObject></p>

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Increased caecal Intestinimonas abundance inhibits E. tenella gametogenesis via EtGFAT regulation and alleviates infection through immunity

  • Jun-Yi Li,
  • Hai-Bin Huang,
  • Chun-Wei Shi,
  • Tian-Xu Pan,
  • Ming-Han Li,
  • Nan Wang,
  • Jia-Jin Shan,
  • Yan-Long Jiang,
  • Wen-Tao Yang,
  • Xin Cao,
  • Jian-Zhong Wang,
  • Jia-Yao Guan,
  • Shu-Yuan Yu,
  • Chun-Feng Wang,
  • Gui-Lian Yang

摘要

Background

Chicken coccidiosis caused by Eimeria tenella (E. tenella) poses a major threat to global poultry production, with its tropism for the caecal microenvironment and dynamic interactions with the resident microbiota remaining incompletely understood. The caecal microbiota plays a critical role in host‒parasite interplay, yet the mechanisms through which microbial homeostasis influences E. tenella development and host resistance remain elusive. This study aimed to elucidate the causal relationship between caecal dysbiosis and E. tenella pathogenesis, with a focus on identifying microbiota-derived regulators of parasite development and host immunity.

Results

Antibiotic-induced caecal dysbiosis (ABX) significantly impaired E. tenella macrogametogenesis, demonstrating microbiota-dependent regulation of parasitic development. Faecal microbiota transplantation (FMT) validated this causal link, revealing that microbial reconstitution restored parasite maturation. Notably, Intestinimonas spp. were identified as key inhibitors of E. tenella development through transcriptional regulation of the EtGFAT gene (Eimeria tenella glucosamine: fructose-6-phosphate aminotransferase), a critical mediator of macrogamete formation. Furthermore, the transplantation of Intestinimonas butyriciproducens (I. butyriciproducens) attenuated clinical manifestations of infection while increasing IFN-γ secretion from CD8+ T lymphocytes, thereby enhancing host resistance to E. tenella.

Conclusions

This study revealed that caecal microbiota homeostasis is indispensable for E. tenella developmental progression and highlights Intestinimonas as a pivotal microbial regulator of parasite biology. The dual role of I. butyriciproducens in suppressing parasitic virulence and potentiating adaptive immune responses underscores the therapeutic potential of microbiota-targeted strategies. These findings provide a foundation for the development of novel anticoccidial interventions through targeted manipulation of caecal microbial communities.

Video Abstract