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空气污染暴露与肌肉骨骼系统的自身炎症性和自身免疫性疾病:流行病学和机制证据的综述。

Air pollution exposure and auto-inflammatory and autoimmune diseases of the musculoskeletal system: a review of epidemiologic and mechanistic evidence.

机构信息

Department of Epidemiology and Biostatistics, School of Public Health, Anhui Medical University, 81 Meishan Road, Hefei, 230032, Anhui, People's Republic of China.

Institute of Kidney Disease, Inflammation and Immunity Mediated Diseases, The Second Hospital of Anhui Medical University, Hefei, 230032, Anhui, People's Republic of China.

出版信息

Environ Geochem Health. 2023 Jul;45(7):4087-4105. doi: 10.1007/s10653-023-01495-x. Epub 2023 Feb 3.

Abstract

Auto-inflammatory and autoimmune diseases of the musculoskeletal system can be perceived as a spectrum of rheumatic diseases, with the joints and connective tissues are eroded severely that progressively develop chronic inflammation and lesion. A wide range of risk factors represented by genetic and environmental factors have been uncovered by population-based surveys and experimental studies. Lately, the exposure to air pollution has been found to be potentially involved in the mechanisms of occurrence or development of such diseases, principally manifest in oxidative stress, local and systemic inflammation, and epigenetic modifications, as well as the mitochondrial dysfunction, which has been reported to participate in the intermediate links. The lungs might serve as a starting area of air pollutants, which would cause oxidative stress-induced bronchial-associated lymphoid tissue (iBALT) to further to influence T, B cells, and the secretion of pro-inflammatory cytokines. The binding of aromatic hydrocarbon receptor (AhR) to the corresponding contaminant ligands tends to regulate the reaction of Th17 and Tregs. Furthermore, air pollution components might spur on immune and inflammatory responses by damaging mitochondria that could interact with and exacerbate oxidative stress and pro-inflammatory cytokines. In this review, we focused on the association between air pollution and typical auto-inflammatory and autoimmune diseases of the musculoskeletal system, mainly including osteoarthritis (OA), rheumatoid arthritis (RA), spondyloarthritis (SpA) and juvenile idiopathic arthritis (JIA), and aim to collate the mechanisms involved and the potential channels. A complete summary and in-depth understanding of the autoimmune and inflammatory effects of air pollution exposure should hopefully contribute new perspectives on how to formulate better public health policies to alleviate the adverse health effects of air pollutants.

摘要

自身炎症性和自身免疫性肌肉骨骼系统疾病可被视为一组风湿性疾病,关节和结缔组织受到严重侵蚀,导致慢性炎症和病变逐渐发展。基于人群的调查和实验研究揭示了广泛的遗传和环境因素等风险因素。最近,发现空气污染暴露可能与这些疾病的发生或发展机制有关,主要表现为氧化应激、局部和全身炎症以及表观遗传修饰,以及线粒体功能障碍,据报道,这些因素参与了中间环节。肺部可能是空气污染物的起始区域,它会导致氧化应激诱导的支气管相关淋巴组织(iBALT)进一步影响 T 细胞、B 细胞和促炎细胞因子的分泌。芳香烃受体(AhR)与相应污染物配体的结合倾向于调节 Th17 和 Tregs 的反应。此外,空气污染成分可能通过损害与氧化应激和促炎细胞因子相互作用并加重其作用的线粒体来刺激免疫和炎症反应。在这篇综述中,我们重点关注了空气污染与肌肉骨骼系统中典型的自身炎症性和自身免疫性疾病(主要包括骨关节炎(OA)、类风湿关节炎(RA)、脊柱关节炎(SpA)和青少年特发性关节炎(JIA))之间的关联,旨在整理所涉及的机制和潜在途径。全面深入地了解空气污染暴露的自身免疫和炎症作用,有望为制定更好的公共卫生政策以减轻空气污染物的不良健康影响提供新的视角。

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