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

被引:19
作者
Zhang, Ruo-Di [1 ,2 ]
Chen, Cong [1 ,2 ]
Wang, Peng [2 ,3 ]
Fang, Yang [1 ,2 ]
Jiang, Ling-Qiong [1 ,2 ]
Fang, Xi [1 ,2 ]
Zhao, Yan [1 ,2 ]
Ni, Jing [1 ,2 ]
Wang, De-Guang [2 ,4 ]
Pan, Hai-Feng [1 ,2 ]
机构
[1] Anhui Med Univ, Sch Publ Hlth, Dept Epidemiol & Biostat, 81 Meishan Rd, Hefei 230032, Anhui, Peoples R China
[2] Anhui Med Univ, Inst Kidney Dis Inflammat & Immun Mediated Dis, Hosp 2, Hefei 230032, Anhui, Peoples R China
[3] Anhui Med Univ, Teaching Ctr Prevent Med, Sch Publ Hlth, 81 Meishan Rd, Hefei 230032, Anhui, Peoples R China
[4] Anhui Med Univ, Hosp 2, Dept Nephrol, Hefei 230032, Anhui, Peoples R China
基金
中国国家自然科学基金;
关键词
Air pollution; Particulate matter; Inflammation; Autoimmune diseases; Mitochondria; JUVENILE IDIOPATHIC ARTHRITIS; ARYL-HYDROCARBON RECEPTOR; KAPPA-B ACTIVATION; RHEUMATOID-ARTHRITIS; PARTICULATE MATTER; OXIDATIVE STRESS; TNF-ALPHA; MITOCHONDRIAL DYSFUNCTION; DNA METHYLATION; CIGARETTE-SMOKE;
D O I
10.1007/s10653-023-01495-x
中图分类号
X [环境科学、安全科学];
学科分类号
08 ; 0830 ;
摘要
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.
引用
收藏
页码:4087 / 4105
页数:19
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