{"title":"Gut-derived immune cells and the gut-lung axis in ARDS.","authors":"Mairi Ziaka, Aristomenis Exadaktylos","doi":"10.1186/s13054-024-05006-x","DOIUrl":null,"url":null,"abstract":"<p><p>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.</p>","PeriodicalId":10811,"journal":{"name":"Critical Care","volume":null,"pages":null},"PeriodicalIF":8.8000,"publicationDate":"2024-07-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11225303/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Critical Care","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1186/s13054-024-05006-x","RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"CRITICAL CARE MEDICINE","Score":null,"Total":0}
引用次数: 0
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.
肠道是一个重要的免疫器官,协调免疫反应并影响远处的粘膜部位,尤其是呼吸道粘膜。人们越来越认识到,肠道是危重疾病的核心驱动因素,肠道高通透性会促进细菌转运、全身炎症和器官损伤。肠道-肺 "轴是一个关键途径,肠道源性损伤因子通过全身循环引发急性肺损伤(ALI)。肠道微生物群的直接和间接影响对免疫反应有重大影响。菌群失调,尤其是肠道菌群失调,被称为微生物物种失衡和某些体内微生物群中微生物多样性的减少,会影响适应性免疫反应,包括分化 T 调节细胞(Tregs)和 T 辅助细胞 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也会影响肺部免疫活动,凸显了肠道与肺部之间复杂的相互作用。此外,肺部微生物群的改变与多种肠道病变有关,影响着局部和全身的免疫环境。值得注意的是,肺部菌群失调会相互影响肠道微生物群的组成,这表明肠道与肺部之间存在双向交流。在这篇综述中,我们研究了 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了免疫细胞在肠道-肺轴中的作用。这一探索旨在加深对 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意义。
期刊介绍:
Critical Care is an esteemed international medical journal that undergoes a rigorous peer-review process to maintain its high quality standards. Its primary objective is to enhance the healthcare services offered to critically ill patients. To achieve this, the journal focuses on gathering, exchanging, disseminating, and endorsing evidence-based information that is highly relevant to intensivists. By doing so, Critical Care seeks to provide a thorough and inclusive examination of the intensive care field.