Evidence map›Paper›PMID 41610307›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026

Neural Circuits between Nodose Ganglion and Pulmonary Neuroendocrine Cells Regulate Lung Inflammatory Responses.

Jie Chen, Shitao Xie, Zhekai Lin, Caiqi Zhao, Rujia Tao, Yingying Ma, Xiaoyan Chen, Renlan Wu, Qingjian Han, Pengfei Sui and 7 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

17 authors.

Jie ChenShanghai Institute of Materia Medica, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai, China.
Shitao XieShanghai Institute of Materia Medica, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai, China.
Zhekai LinShanghai Institute of Materia Medica, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai, China.
Caiqi ZhaoShanghai Institute of Materia Medica, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai, China.
Rujia TaoShanghai Institute of Materia Medica, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai, China.
Yingying MaShanghai Institute of Materia Medica, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai, China.
Xiaoyan ChenShanghai Key Laboratory of Lung Inflammation and Injury, Department of Pulmonary Medicine, Zhongshan Hospital, Fudan University, Shanghai, China.
Renlan WuShanghai Institute of Materia Medica, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai, China.
Qingjian HanInstitutes of Brain Science, Fudan University, Shanghai, China.
Pengfei SuiShanghai Institute of Biochemistry and Cell Biology, Chinese Academy of Sciences, Shanghai, China.
Sheng WangDepartment of Neurobiology, Hebei Medical University, Hebei, China.
Hongbin JiShanghai Institute of Biochemistry and Cell Biology, Chinese Academy of Sciences, Shanghai, China.
Hai SongThe MOE Key Laboratory of Biosystems Homeostasis and Protection, Zhejiang Provincial Key Laboratory for Cancer Molecular Cell Biology and Innovation Center for Cell Signaling Network, Life Sciences Institute, Zhejiang University, Hangzhou, Zhejiang, China.
Xiaoming ZhangShanghai Institute of Materia Medica, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai, China.
Yangang SunInstitute of Neuroscience, State Key Laboratory of Neuroscience, Center for Excellence in Brain Science & Intelligence Technology, Chinese Academy of Sciences, Shanghai, China.
Yuanlin SongShanghai Key Laboratory of Lung Inflammation and Injury, Department of Pulmonary Medicine, Zhongshan Hospital, Fudan University, Shanghai, China.
Xiao SuShanghai Institute of Materia Medica, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai, China.ORCID https://orcid.org/0000-0002-8692-8365

Funding

China Postdoctoral Science Foundation 2024M750522Key Technologies Research and Development Program 2022YFC2304702NSFC 82241042NSFC 82400103NSFC 82495200/02Science and Technology Commission of Shanghai Municipality 20DZ2261200
6 · The paper itself

Abstract

The lungs interface directly with the external environment, exposing them to airborne pathogens like endotoxins. We investigated whether the vagus nerve, which innervates the lungs-detects such pathogens. Using transcriptomics, tissue clearance imaging, electrophysiology, and cell-specific knockout models, we discovered that vagal sensory endings synapse with pulmonary neuroendocrine cells (PNECs). These nerve endings detect bacterial endotoxins primarily through the pain receptor TRPA1, not via Toll-like receptor 4 (TLR4). This detection triggers electrical excitation in vagal neurons and upregulates neuropeptide (e.g., αCGRP) production in the nodose ganglia. Released αCGRP then acts back on PNECs, stimulating their neuropeptide synthesis and proliferation. This creates a feed-forward loop that amplifies endotoxin-induced lung inflammation. Our findings reveal a critical neural circuit between the nodose ganglion and PNECs that regulates pulmonary inflammatory responses.

Indexed as

LungNeuroendocrine CellsNodose GanglionPneumoniaAnimalsMiceVagus Nervealpha‐calcitonin gene related peptide (αCGRP)pathogen recognitionpulmonary neuroendocrine cells (PNECs)transient receptor potential ankyin1 (TRPA1)vagal nodose sensory neurons

Identifiers

PMID41610307
PMCPMC12948239

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.