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

Abstract 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.