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Gut-derived immune cells and the gut-lung axis in ARDS
Critical Care ( IF 8.8 ) Pub Date : 2024-07-04 , DOI: 10.1186/s13054-024-05006-x Mairi Ziaka 1, 2 , Aristomenis Exadaktylos 2
Critical Care ( IF 8.8 ) Pub Date : 2024-07-04 , DOI: 10.1186/s13054-024-05006-x Mairi Ziaka 1, 2 , Aristomenis Exadaktylos 2
Affiliation
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.
中文翻译:
ARDS 中的肠源性免疫细胞和肠肺轴
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,特别是呼吸道粘膜。它越来越被认为是危重疾病的主要驱动因素,肠道渗透性过高会促进细菌移位、全身炎症和器官损伤。 “肠-肺”轴成为一条关键通路,肠道源性有害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影响显着影响免疫反应。菌群失调,特别是肠道菌群失调,被称为微生物物种失衡和某些身体微生物组内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 (Treg) 和辅助性 T 17 (Th17) 细胞,这对于免疫系统至关重要。各种肺部炎症。此外,肠道和骨髓免疫细胞影响肺部免疫活动,强调了复杂的肠肺相互作用。此外,肺部微生物群的改变与多种肠道病理有关,影响局部和全身免疫景观。值得注意的是,肺生态失调可以相互影响肠道微生物群的组成,表明肠-肺之间存在双向沟通。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肺轴中的作用。这项探索旨在加深对 ALI/ARDS 发病机制的了解,并强调肠-肺相互作用在呼吸系统疾病中的重要性。
更新日期:2024-07-05
中文翻译:
ARDS 中的肠源性免疫细胞和肠肺轴
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,特别是呼吸道粘膜。它越来越被认为是危重疾病的主要驱动因素,肠道渗透性过高会促进细菌移位、全身炎症和器官损伤。 “肠-肺”轴成为一条关键通路,肠道源性有害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影响显着影响免疫反应。菌群失调,特别是肠道菌群失调,被称为微生物物种失衡和某些身体微生物组内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 (Treg) 和辅助性 T 17 (Th17) 细胞,这对于免疫系统至关重要。各种肺部炎症。此外,肠道和骨髓免疫细胞影响肺部免疫活动,强调了复杂的肠肺相互作用。此外,肺部微生物群的改变与多种肠道病理有关,影响局部和全身免疫景观。值得注意的是,肺生态失调可以相互影响肠道微生物群的组成,表明肠-肺之间存在双向沟通。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肺轴中的作用。这项探索旨在加深对 ALI/ARDS 发病机制的了解,并强调肠-肺相互作用在呼吸系统疾病中的重要性。