A mouse protozoan boosts antigen-specific mucosal IgA responses in a specific lipid metabolism- and signaling-dependent manner

Yanbo Kou, Shenghan Zhang, Junru Chen, Yusi Shen, Zhiwei Zhang, Haohan Huang, Yulu Ma, Yaoyao Xiang, Longxiang Liao, Junyang Zhou, Wanpeng Cheng, Yuan Zhou, Huan Yang, Zhuanzhuan Liu, Yanxia Wei, Hui Wang and Yugang Wang ()
Additional contact information
Yanbo Kou: Xuzhou Medical University
Shenghan Zhang: Xuzhou Medical University
Junru Chen: Xuzhou Medical University
Yusi Shen: Xuzhou Medical University
Zhiwei Zhang: Xuzhou Medical University
Haohan Huang: Xuzhou Medical University
Yulu Ma: Xuzhou Medical University
Yaoyao Xiang: Xuzhou Medical University
Longxiang Liao: Xuzhou Medical University
Junyang Zhou: Xuzhou Medical University
Wanpeng Cheng: Xuzhou Medical University
Yuan Zhou: Xuzhou Medical University
Huan Yang: Xuzhou Medical University
Zhuanzhuan Liu: Xuzhou Medical University
Yanxia Wei: Xuzhou Medical University
Hui Wang: Xuzhou Medical University
Yugang Wang: Xuzhou Medical University

Nature Communications, 2024, vol. 15, issue 1, 1-19

Abstract: Abstract IgA antibodies play an important role in mucosal immunity. However, there is still no effective way to consistently boost mucosal IgA responses, and the factors influencing these responses are not fully understood. We observed that colonization with the murine intestinal symbiotic protozoan Tritrichomonas musculis (T.mu) boosted antigen-specific mucosal IgA responses in wild-type C57BL/6 mice. This enhancement was attributed to the accumulation of free arachidonic acid (ARA) in the intestinal lumen, which served as a signal to stimulate the production of antigen-specific mucosal IgA. When ARA was prevented from undergoing its downstream metabolic transformation using the 5-lipoxygenase inhibitor zileuton or by blocking its downstream biological signaling through genetic deletion of the Leukotriene B4 receptor 1 (Blt1), the T.mu-mediated enhancement of antigen-specific mucosal IgA production was suppressed. Moreover, both T.mu transfer and dietary supplementation of ARA augmented the efficacy of an oral vaccine against Salmonella infection, with this effect being dependent on Blt1. Our findings elucidate a tripartite circuit linking nutrients from the diet or intestinal microbiota, host lipid metabolism, and the mucosal humoral immune response.

Date: 2024
References: View references in EconPapers View complete reference list from CitEc
Citations:

Downloads: (external link)
https://www.nature.com/articles/s41467-024-52336-z Abstract (text/html)

Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.

Export reference: BibTeX RIS (EndNote, ProCite, RefMan) HTML/Text

Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:15:y:2024:i:1:d:10.1038_s41467-024-52336-z

Ordering information: This journal article can be ordered from
https://www.nature.com/ncomms/

DOI: 10.1038/s41467-024-52336-z

Access Statistics for this article

Nature Communications is currently edited by Nathalie Le Bot, Enda Bergin and Fiona Gillespie

More articles in Nature Communications from Nature
Bibliographic data for series maintained by Sonal Shukla () and Springer Nature Abstracting and Indexing ().