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STING Promotes Intestinal IgA Production by Regulating Acetate-producing Bacteria to Maintain Host-microbiota
Tianming Yu1,2, Wenjing Yang1,2, Suxia Yao1,2
1Department of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX 77555, USA.
Inflammatory Bowel Diseases
|January 20, 2023
Summary
The STING pathway regulates intestinal IgA production by influencing acetate-producing gut bacteria. Impaired STING function in mice led to reduced IgA and altered gut microbiota, which acetate supplementation could restore.
Area of Science:
- Immunology
- Microbiology
- Gastroenterology
Background:
- Intestinal Immunoglobulin A (IgA) is vital for host-microbiota balance and gut health.
- The cGAS-STING pathway is activated by gut bacteria, but its role in intestinal IgA is unclear.
Purpose of the Study:
- To investigate the role of STING in regulating intestinal IgA response.
- To understand the mechanisms by which STING influences IgA production.
Main Methods:
- Compared IgA levels in wild-type and Sting-/- mice during homeostasis and infection.
- Utilized STING agonists, 16S rRNA gene sequencing, metabolomics, and fecal microbiota transfer.
- Assessed short-chain fatty acid (SCFA) levels and GPR43 mediation.
Main Results:
- Sting-/- mice showed impaired intestinal IgA response.
- STING agonists did not directly activate B cells or dendritic cells for IgA induction.
- Sting-/- mice exhibited altered gut microbiota, decreased SCFA-producing bacteria, and reduced SCFA fermentation.
- Fecal transfer from Sting-/- mice resulted in lower IgA, mediated by GPR43.
- Acetate supplementation restored IgA production in Sting-/- mice.
Conclusions:
- STING signaling is crucial for maintaining intestinal IgA levels.
- STING promotes IgA production indirectly by regulating acetate-producing gut bacteria.
- Acetate plays a key role in STING-mediated intestinal IgA regulation.
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