Mesh : Humans Respiratory Distress Syndrome / immunology physiopathology microbiology Gastrointestinal Microbiome / physiology immunology Lung / immunology physiopathology microbiology Dysbiosis / physiopathology immunology complications Animals

来  源:   DOI:10.1186/s13054-024-05006-x   PDF(Pubmed)

Abstract:
The gut serves as a vital immunological organ orchestrating immune responses and influencing distant mucosal sites, notably the respiratory mucosa. It is increasingly recognized as a central driver of critical illnesses, with intestinal hyperpermeability facilitating bacterial translocation, systemic inflammation, and organ damage. The \"gut-lung\" axis emerges as a pivotal pathway, where gut-derived injurious factors trigger acute lung injury (ALI) through the systemic circulation. Direct and indirect effects of gut microbiota significantly impact immune responses. Dysbiosis, particularly intestinal dysbiosis, termed as an imbalance of microbial species and a reduction in microbial diversity within certain bodily microbiomes, influences adaptive immune responses, including differentiating T regulatory cells (Tregs) and T helper 17 (Th17) cells, which are critical in various lung inflammatory conditions. Additionally, gut and bone marrow immune cells impact pulmonary immune activity, underscoring the complex gut-lung interplay. Moreover, lung microbiota alterations are implicated in diverse gut pathologies, affecting local and systemic immune landscapes. Notably, lung dysbiosis can reciprocally influence gut microbiota composition, indicating bidirectional gut-lung communication. In this review, we investigate the pathophysiology of ALI/acute respiratory distress syndrome (ARDS), elucidating the role of immune cells in the gut-lung axis based on recent experimental and clinical research. This exploration aims to enhance understanding of ALI/ARDS pathogenesis and to underscore the significance of gut-lung interactions in respiratory diseases.
摘要:
肠道作为重要的免疫器官,协调免疫反应并影响远处的粘膜部位。尤其是呼吸道粘膜。它越来越被认为是严重疾病的核心驱动力,肠道通透性过高促进细菌移位,全身性炎症,和器官损伤。“肠-肺”轴是一条关键途径,肠源性损伤因素通过体循环引发急性肺损伤(ALI)。肠道微生物群的直接和间接作用显著影响免疫反应。菌群失调,特别是肠道生态失调,被称为微生物物种的不平衡和某些身体微生物群落中微生物多样性的减少,影响适应性免疫反应,包括分化的调节性T细胞(Tregs)和辅助性T细胞17(Th17),这在各种肺部炎症中至关重要。此外,肠道和骨髓免疫细胞影响肺免疫活性,强调复杂的肠-肺相互作用。此外,肺微生物群的改变与不同的肠道病理有关,影响局部和全身免疫景观。值得注意的是,肺菌群失调可以相互影响肠道菌群组成,指示双向肠-肺通讯。在这次审查中,我们调查了ALI/急性呼吸窘迫综合征(ARDS)的病理生理学,根据最近的实验和临床研究,阐明免疫细胞在肠-肺轴中的作用。这项探索旨在增强对ALI/ARDS发病机制的理解,并强调肠-肺相互作用在呼吸系统疾病中的重要性。
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