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患者肺部与肠道之间的复杂相互作用:揭示其串扰机制。

The intricate interactions between the lungs and gut in patients: unraveling the crosstalk mechanism.

作者信息

Li Jiale, Chen Yiting, Hu Bangchuan

机构信息

The Second Clinical Medical College, Zhejiang Chinese Medical University, Hangzhou, China.

Emergency and Critical Care Center, ICU, Zhejiang Provincial People's Hospital (Affiliated People's Hospital, Hangzhou Medical College), Hangzhou, Zhejiang, China.

出版信息

Front Med (Lausanne). 2025 Jul 30;12:1624907. doi: 10.3389/fmed.2025.1624907. eCollection 2025.


DOI:10.3389/fmed.2025.1624907
PMID:40809439
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12343513/
Abstract

There is a growing body of evidence indicating that the stimulation of one organ can significantly influence the functioning of another. For instance, intestinal complications are frequently observed during respiratory diseases, and conversely, pulmonary complications can arise during intestinal diseases-a phenomenon referred to as lung-gut crosstalk. Patients suffering from mechanical ventilator-induced lung injury, chronic obstructive pulmonary disease (COPD), acute respiratory distress syndrome (ARDS), and other pulmonary conditions have been shown to experience gastrointestinal dysfunction and related disorders. Similarly, individuals with inflammatory bowel disease (IBD) have also been found to develop pulmonary complications. However, these studies are not enough to fully explain the mechanism of lung-intestinal crosstalk, and more potential mechanisms need to be explored and further elucidated. In this paper, we summarize recent research advancements regarding lung-intestinal interactions in the context of pulmonary and intestinal diseases, analyzing the potential mechanisms of lung-intestinal crosstalk from the perspectives of respiratory mechanics, inflammation, and microbiota. Additionally, we review evidence suggesting that adipokines may play a role in lung-gut interactions, and we propose new avenues for investigating the mechanisms underlying these interactions.

摘要

越来越多的证据表明,一个器官受到刺激会显著影响另一个器官的功能。例如,在呼吸系统疾病期间经常观察到肠道并发症,反之,在肠道疾病期间也可能出现肺部并发症——这种现象被称为肺-肠串扰。患有机械通气诱导性肺损伤、慢性阻塞性肺疾病(COPD)、急性呼吸窘迫综合征(ARDS)和其他肺部疾病的患者已被证明会出现胃肠功能障碍及相关病症。同样,患有炎症性肠病(IBD)的个体也被发现会出现肺部并发症。然而,这些研究不足以完全解释肺-肠串扰的机制,还需要探索和进一步阐明更多潜在机制。在本文中,我们总结了近期在肺部和肠道疾病背景下关于肺-肠相互作用的研究进展,从呼吸力学、炎症和微生物群的角度分析肺-肠串扰的潜在机制。此外,我们回顾了表明脂肪因子可能在肺-肠相互作用中起作用的证据,并提出了研究这些相互作用潜在机制的新途径。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/66c5/12343513/0d6a0d2d9b64/fmed-12-1624907-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/66c5/12343513/1126e413ef8a/fmed-12-1624907-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/66c5/12343513/2e3c29b64c80/fmed-12-1624907-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/66c5/12343513/0d6a0d2d9b64/fmed-12-1624907-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/66c5/12343513/1126e413ef8a/fmed-12-1624907-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/66c5/12343513/2e3c29b64c80/fmed-12-1624907-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/66c5/12343513/0d6a0d2d9b64/fmed-12-1624907-g003.jpg

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本文引用的文献

[1]
British Society of Gastroenterology guidelines on inflammatory bowel disease in adults: 2025.

Gut. 2025-6-23

[2]
Lung microbiota: a new hope for treating acute respiratory distress syndrome?

Front Microbiol. 2025-5-30

[3]
The release and cytotoxicity of novel light inducible antimicrobial coatings after incineration.

Ecotoxicol Environ Saf. 2025-7-15

[4]
The double-edged sword of metabolic and bariatric surgery: extending the biliary limb can trigger bacterial translocation, sepsis, and liver inflammation - an experimental study.

Int J Surg. 2025-7-1

[5]
Intestinal IL-17 family orchestrates microbiota-driven histone deacetylation and promotes Treg differentiation to mediate the alleviation of asthma by Ma-Xing-Shi-Gan decoction.

Phytomedicine. 2025-7

[6]
Exogenous acetate mitigates later enhanced allergic airway inflammation in a menopausal mouse model.

Front Cell Infect Microbiol. 2025-4-10

[7]
Antimicrobial potential of biopolymers against foodborne pathogens: An updated review.

Microb Pathog. 2025-7

[8]
Macrophage peroxisomes guide alveolar regeneration and limit SARS-CoV-2 tissue sequelae.

Science. 2025-3-7

[9]
Inhibition of macrophage inflammasome assembly and pyroptosis with GC-1 ameliorates acute lung injury.

Theranostics. 2025-1-20

[10]
Type 2 immunity in allergic diseases.

Cell Mol Immunol. 2025-3

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