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Peer-reviewedCC BY-NC-ND 4.0Proceedings of the National Academy of Sciences of the United States of America

Gut microbiota vesicle reprogramming by Ganoderma lucidum polysaccharide alleviates mycoplasmal pneumonia via the gut–lung axis

  • Zimu Zhang1
  • Hanfei Gong1,2,3
  • Zhenzhen Zhang2,3
  • Ping Ying4
  • Chao Zhang1
  • Wenjun Xu1
  • Lingyi Kong1
4 affiliations
  1. 1Joint International Research Laboratory of Target Discovery and New Drug Innovation, Ministry of Education, State Key Laboratory of Natural Medicines, and Jiangsu Key Laboratory of Bioactive Natural Product Research, China Pharmaceutical University, Nanjing 211198, China
  2. 2Institute of Veterinary Medicine, Jiangsu Academy of Agricultural Sciences, Nanjing 210014, China
  3. 3Guo’Tai (Taizhou) Center of Technology Innovation for Veterinary Biologicals, Taizhou 225300, China
  4. 4Modern Industrial College of Traditional Chinese Medicine and Health, Lishui University, Lishui 323000, China
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Abstract

Respiratory infections remain a major global health challenge, further compounded by antibiotic resistance. Among these, mycoplasmal pneumonia represents a particularly prevalent and refractory form. Here, using targeted enzymatic fragmentation combined with multidimensional NMR analysis, we resolved the structure of a homogeneous Ganoderma lucidum polysaccharide, GLFP2, and identified β-(1→6)-linked galactosyl motifs as key structural features. Despite minimal systemic absorption, oral GLFP2 alleviated mycoplasmal pneumonia in mice. Instead, GLFP2 reshaped the gut microbiota and functionally reprogrammed gut microbiota-derived extracellular vesicles (GMEVs), whose transplantation alone was sufficient to confer pulmonary protection. Orally administered GMEVs remained bioactive, showed systemic exposure, associated with the lung, and were preferentially taken up by alveolar macrophages. These vesicles activated AMP-activated protein kinase (AMPK) signaling, suppressed the S100A8/A9 inflammatory axis, and limited neutrophil-driven immunopathology. Collectively, these findings identify microbiota-derived vesicles as effectors of gut–lung communication and use a defined polysaccharide to uncover a remote protective mechanism against pneumonia.

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Cite

BibTeXRIS
BibTeX
@article{zhang2026microbiota,
  title = {{Gut microbiota vesicle reprogramming by Ganoderma lucidum polysaccharide alleviates mycoplasmal pneumonia via the gut–lung axis}},
  author = {Zimu Zhang and Hanfei Gong and Zhenzhen Zhang and Ping Ying and Chao Zhang and Wenjun Xu and Lingyi Kong},
  journal = {Proceedings of the National Academy of Sciences of the United States of America},
  year = {2026},
  month = oct,
  doi = {10.1073/pnas.2603618123},
  url = {https://doi.org/10.1073/pnas.2603618123},
  note = {CC BY-NC-ND 4.0},
}
RIS
TY  - JOUR
TI  - Gut microbiota vesicle reprogramming by Ganoderma lucidum polysaccharide alleviates mycoplasmal pneumonia via the gut–lung axis
AU  - Zimu Zhang
AU  - Hanfei Gong
AU  - Zhenzhen Zhang
AU  - Ping Ying
AU  - Chao Zhang
AU  - Wenjun Xu
AU  - Lingyi Kong
PY  - 2026
DA  - 2026/10/20
JO  - Proceedings of the National Academy of Sciences of the United States of America
DO  - 10.1073/pnas.2603618123
UR  - https://doi.org/10.1073/pnas.2603618123
AB  - Respiratory infections remain a major global health challenge, further compounded by antibiotic resistance. Among these, mycoplasmal pneumonia represents a particularly prevalent and refractory form. Here, using targeted enzymatic fragmentation combined with multidimensional NMR analysis, we resolved the structure of a homogeneous Ganoderma lucidum polysaccharide, GLFP2, and identified β-(1→6)-linked galactosyl motifs as key structural features. Despite minimal systemic absorption, oral GLFP2 alleviated mycoplasmal pneumonia in mice. Instead, GLFP2 reshaped the gut microbiota and functionally reprogrammed gut microbiota-derived extracellular vesicles (GMEVs), whose transplantation alone was sufficient to confer pulmonary protection. Orally administered GMEVs remained bioactive, showed systemic exposure, associated with the lung, and were preferentially taken up by alveolar macrophages. These vesicles activated AMP-activated protein kinase (AMPK) signaling, suppressed the S100A8/A9 inflammatory axis, and limited neutrophil-driven immunopathology. Collectively, these findings identify microbiota-derived vesicles as effectors of gut–lung communication and use a defined polysaccharide to uncover a remote protective mechanism against pneumonia.
SN  - 0027-8424
SN  - 1091-6490
ER  -