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Updated: Jul 15, 2025

Induction of Intestinal Inflammation by Adoptive Transfer of CBir1 TCR Transgenic CD4+ T Cells to Immunodeficient Mice
Published on: December 16, 2021
Gut microbiota-derived autoinducer-2 regulates lung inflammation through the gut-lung axis
Xianghao Zeng1, Huawen Yue2, Ling Zhang2
1Clinical Medical College, North Sichuan Medical College, Nanchong City, Sichuan Province 637000, China; Department of Gastroenterology, Clinical Medical College and the First Affiliated Hospital of Chengdu Medical College, Chengdu City, Sichuan Province 610500, China.
Gut bacteria produce autoinducer-2 (AI-2), a molecule that influences lung inflammation via the gut-lung axis. This study shows AI-2 exacerbates lung injury, suggesting it as a therapeutic target.
Area of Science:
- Microbiology
- Immunology
- Gastroenterology
Background:
- Autoinducer-2 (AI-2) is a bacterial quorum sensing molecule.
- The gut-lung axis describes bidirectional communication between the gut and lungs.
- The role of AI-2 in lung immunity via the gut-lung axis is not well understood.
Purpose of the Study:
- To investigate the involvement of AI-2 in lung immunity through the gut-lung axis.
- To determine if AI-2 influences lung inflammation.
Main Methods:
- Analyzed AI-2 levels and gut microbiome composition in stool samples from pneumonic patients and an acute lung injury mouse model.
- Investigated the effect of AI-2 on lung inflammation in the mouse model.
Main Results:
- Reduced gut microbiota diversity was observed in pneumonic patients receiving antibiotics.
- AI-2 levels in stool correlated positively with serum inflammatory molecules in pneumonic patients.
- AI-2 administration exacerbated lung inflammation in mice, increasing inflammatory cytokine and chemokine secretion.
- An AI-2 inhibitor, D-ribose, alleviated AI-2-induced lung inflammation.
Conclusions:
- Gut microbiota-derived AI-2 plays a role in modulating lung inflammation.
- AI-2 may represent a therapeutic target for lung inflammatory diseases via the gut-lung axis.
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