- Title
- The role of gut-lung axis in COPD: Pathogenesis, immune response, and prospective treatment
- Creator
- Song, Zhi; Meng, Yifei; Fricker, Michael; Li, Xin'ao; Tian, Haochen; Tan, Yurong; Qin, Ling
- Relation
- Heliyon Vol. 10, Issue 9, no. e30612
- Publisher Link
- http://dx.doi.org/10.1016/j.heliyon.2024.e30612
- Publisher
- Elsevier
- Resource Type
- journal article
- Date
- 2024
- Description
- Chronic obstructive pulmonary disease (COPD) is a major cause of morbidity and healthcare burden worldwide. The progression of COPD is a combination of genetic predisposition and environmental factors, primarily cigarette smoking, and the underlying mechanisms are still unknown. Intestinal microecology impacts host immunity, metabolism, and resistance to pathogenic infections, which may be involved in pulmonary disease. Moreover, substantial interaction occurs between the intestinal and respiratory immune niches. After reviewing nearly 500 articles, we found the gut-lung axis plays an important role in the development of COPD. COPD patients often have dysbiosis of the intestinal microenvironment, which can affect host immunity through a series of mechanisms, exacerbating or protecting against COPD progression. This paper summarizes how the gut-lung axis influences COPD, including the alterations of intestinal microecology, the pathological mechanisms, and the involved immune responses. Finally, we summarize the latest research advances in COPD treatment from the perspective of regulating the gut-lung axis and intestinal immunity and evaluate the potential value of the gut-lung axis in improving COPD prognosis.
- Subject
- chronic obstructive pulmonary disease (COPD); gut-lung axis; intestinal microenvironment; muscosal immune
- Identifier
- http://hdl.handle.net/1959.13/1503828
- Identifier
- uon:55409
- Identifier
- ISSN:2405-8440
- Rights
- © 2024 The Authors. Published by Elsevier Ltd. This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).
- Language
- eng
- Full Text
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