Interleukin-1β exacerbates Eimeria tenella-induced cecal inflammation by disrupting intestinal barrier integrity and enhancing inflammatory mediator expression.

Authors

Xiaoling Lv, Jiaqi Zhao, Baojie Li, Xuan Chang, Sichen Dong, Menggang Li, Kewei Dou, Rui Bai, Li Zhang, Xiaozhen Cui, Mingxue Zheng

Published in

Veterinary parasitology. Volume 349. Pages 110954. Oct 18, 2026. Epub Oct 18, 2026.

Abstract

Eimeria tenella is a highly pathogenic protozoan parasite that causes severe hemorrhagic cecitis in chickens, leading to substantial economic losses to the global poultry industry. Interleukin-1β (IL-1β), a master regulator of inflammation, is strongly upregulated during E. tenella infection; however, its precise functional role in cecal inflammation remains unclear. In this study, recombinant chicken IL-1β and IL-6 proteins were expressed and purified using a prokaryotic expression system. Hyperimmune sera against IL-1β and IL-6 were generated in specific pathogen-free (SPF) chickens and administered passively to E. tenella-infected chickens. Clinical outcomes, cecal histopathology, ultrastructure using transmission electron microscopy, and expression of inflammatory mediators were evaluated. Neutralization of IL-1β or IL-6 significantly improved weight gain, reduced cecal lesion scores, and eliminated mortality in infected chickens. Ultrastructural analysis revealed that IL-1β neutralization preserved tight junction integrity and microvilli architecture in cecal epithelial cells. Mechanistically, IL-1β promoted inflammation by upregulating the expression of IL-6, IL-8, claudin-2, leukotriene D4 (LTD4), myeloperoxidase (MPO), and von Willebrand factor (vWF), while suppressing sealing tight junction proteins ZO‑1 and Occludin; neutralization of IL‑1β or IL‑6 significantly restored their expression. Combined neutralization of both IL-1β and IL-6 provided superior protection compared to single cytokine neutralization. These findings demonstrate that IL-1β plays a detrimental role in E. tenella-induced cecal inflammation by disrupting intestinal barrier integrity and amplifying inflammatory cascades, suggesting that targeting the IL-1β/IL-6 axis represents a potential therapeutic strategy for mitigating coccidiosis-induced pathology.

PMID:
42913127
Bibliographic data and abstract were imported from PubMed on 24 Oct 2026.

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