ArticleJournal of inflammation research2025
Maxing Shigan Decoction Alleviates Lung Heat Syndrome by Inhibiting α4β7-Mediated γδT17 Cell Migration Across the Gut-Lung-Nasal Axis.
Article in Journal of inflammation research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Gut microbiota as a therapeutic target of Chinese herbal medicine in allergic rhinitis: the gut-nasal axis and immunity.Frontiers in physiology · 2026Review
- Insights into the mechanism of intestinal flora imbalance and immune disorder in co-morbidity of pneumonia and diarrhea in children.Frontiers in pediatrics · 2026Review
- Key messengers in the gut-nose axis: mechanisms of gut microbial metabolites in the immunomodulation of allergic rhinitis.Frontiers in immunology · 2026Review
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Purpose: Lung Heat Syndrome (LHS), a pathological state in Traditional Chinese Medicine characterized by pulmonary inflammation, lacks mechanistic understanding of its gut-lung-nasal axis involvement. Maxing Shigan decoction (MXSGD) clinically resolves LHS, but its immunomodulatory mechanisms remain unclear. This study aimed to elucidate the specific immunomodulatory mechanism through which MXSGD alleviates LHS, focusing on its role in regulating γδT17 cell migration along the gut-lung-nasal axis via the α4β7 pathway. Methods: Network pharmacology and molecular docking identified MXSGD's bioactive components and targets. Mice were randomized into Control, LHS, and different doses of MXSGD groups. LHS was induced by cold stress with intratracheal lipopolysaccharide, and MXSGD was administered orally. Water intake, respiratory rate, and locomotor activity were monitored. CFSE-labeled γδT17 cells were adoptively transferred. CCL25 levels were manipulated using recombinant protein or neutralizing antibody, and α4β7 integrin was blocked with specific antibody. Tissues were analyzed by H&E staining, flow cytometry, ELISA and RT-PCR. Results: Network pharmacology analysis identified 142 shared targets between MXSGD and LHS, with significant enrichment in interleukin-17A (IL-17A) and T cell receptor signaling pathways. MXSGD significantly alleviated reduced water intake and attenuated neutrophil infiltration in ileum and lung. MXSGD inhibited γδT17 cell migration in the lungs and nose, while downregulating IL-17A production in the ileum and lungs and RORγt expression across all tissues. Recombinant CCL25 increased the frequencies of γδT17 cells in the ileum and lungs and α4β7 Conclusion: MXSGD alleviated LHS by inhibiting CCL25/α4β7-dependent γδT17 cell migration and IL-17 production. The study demonstrated γδT17 trafficking as the cellular basis for gut-lung-nasal axis interaction in LHS, while positioning MXSGD as a promising therapy for IL-17-driven respiratory inflammation.
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