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肠道微生物群通过肠-肺轴在调节肺部对病毒感染的免疫反应中的作用。

The Role of Gut Microbiota in the Modulation of Pulmonary Immune Response to Viral Infection Through the Gut-Lung Axis.

作者信息

Chen Na, Li Lianke, Han Yanhua, Chen Zhu

机构信息

Department of Pediatrics, The Second Affiliated Hospital of Guizhou University of Chinese Medicine, Guiyang, Guizhou, 550003, People's Republic of China.

Department of Graduate School, Guizhou University of Traditional Chinese Medicine, Guiyang, Guizhou, 550003, People's Republic of China.

出版信息

J Inflamm Res. 2025 Aug 26;18:11755-11781. doi: 10.2147/JIR.S525880. eCollection 2025.

DOI:10.2147/JIR.S525880
PMID:40901024
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12399867/
Abstract

Viral respiratory infections, including influenza, respiratory syncytial virus (RSV), and SARS-CoV-2, remain major global health challenges due to their high morbidity and mortality. Emerging evidence highlights the pivotal role of the gut-lung axis in regulating pulmonary immunity. The gut microbiota communicates with the lungs via endocrine, immune, and neuroimmune pathways-particularly through metabolites such as short-chain fatty acids (SCFAs) and vagus nerve-mediated signaling-which modulate immune cells including alveolar macrophages and dendritic cells. Disruption of gut microbial balance has been linked to impaired pulmonary immune responses and increased susceptibility to infection. This review synthesizes findings from animal models and clinical studies, demonstrating that interventions such as probiotics (eg, ), prebiotics (eg, ), fecal microbiota transplantation (FMT), and Traditional Chinese Medicine (eg, ) can enhance antiviral cytokine production, restore gut-lung homeostasis, and reduce lung inflammation. For example, FMT from H7N9-survivor mice improved influenza resistance in recipients, and oral probiotics reduced respiratory failure risk in COVID-19 patients. These findings suggest that gut-lung axis modulation is a promising adjunctive approach for treating viral respiratory infections. Future research should prioritize personalized microbiome-based therapies and large-scale clinical trials to validate efficacy and safety.

摘要

包括流感、呼吸道合胞病毒(RSV)和严重急性呼吸综合征冠状病毒2(SARS-CoV-2)在内的病毒性呼吸道感染,因其高发病率和死亡率,仍然是全球主要的健康挑战。新出现的证据凸显了肠-肺轴在调节肺部免疫中的关键作用。肠道微生物群通过内分泌、免疫和神经免疫途径与肺部进行交流,特别是通过短链脂肪酸(SCFAs)等代谢产物和迷走神经介导的信号传导,这些途径调节包括肺泡巨噬细胞和树突状细胞在内的免疫细胞。肠道微生物平衡的破坏与肺部免疫反应受损和感染易感性增加有关。本综述综合了动物模型和临床研究的结果,表明益生菌(如 )、益生元(如 )、粪便微生物群移植(FMT)和传统中药(如 )等干预措施可以增强抗病毒细胞因子的产生,恢复肠-肺稳态,并减轻肺部炎症。例如,来自H7N9幸存者小鼠的粪便微生物群移植提高了受体对流感的抵抗力,口服益生菌降低了COVID-19患者呼吸衰竭的风险。这些发现表明,调节肠-肺轴是治疗病毒性呼吸道感染的一种有前景的辅助方法。未来的研究应优先考虑基于个性化微生物群的疗法和大规模临床试验,以验证其疗效和安全性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/200b/12399867/eeb913190137/JIR-18-11755-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/200b/12399867/45481b7ce188/JIR-18-11755-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/200b/12399867/eeb913190137/JIR-18-11755-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/200b/12399867/45481b7ce188/JIR-18-11755-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/200b/12399867/eeb913190137/JIR-18-11755-g0002.jpg

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本文引用的文献

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Commun Med (Lond). 2024 Nov 22;4(1):244. doi: 10.1038/s43856-024-00633-5.
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Molecular mimicry as a mechanism of viral immune evasion and autoimmunity.分子模拟作为病毒免疫逃逸和自身免疫的一种机制。
Nat Commun. 2024 Oct 30;15(1):9403. doi: 10.1038/s41467-024-53658-8.
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Respiratory syncytial virus (RSV) vaccine effectiveness against RSV-associated hospitalisations and emergency department encounters among adults aged 60 years and older in the USA, October, 2023, to March, 2024: a test-negative design analysis.
呼吸道合胞病毒(RSV)疫苗对美国 60 岁及以上成年人因 RSV 相关住院和急诊就诊的有效性,2023 年 10 月至 2024 年 3 月:一项阴性检测设计分析。
Lancet. 2024 Oct 19;404(10462):1547-1559. doi: 10.1016/S0140-6736(24)01738-0.
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Vaccines for Respiratory Viruses-COVID and Beyond.呼吸道病毒疫苗——新冠及其他。
Vaccines (Basel). 2024 Aug 22;12(8):936. doi: 10.3390/vaccines12080936.
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TLR3/TRIF and MAVS Signaling Is Essential in Regulating Mucosal T Cell Responses during Rotavirus Infection.TLR3/TRIF 和 MAVS 信号在调节轮状病毒感染期间黏膜 T 细胞反应中是必不可少的。
J Immunol. 2024 Oct 1;213(7):1008-1022. doi: 10.4049/jimmunol.2300867.
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