Inflammatory Arthritis and the Environment: Causes and Consequences of Spondyloarthritis.

IF 3 3区 医学 Q2 HEALTH CARE SCIENCES & SERVICES
Maurizio Benucci, Edda Russo, Francesca Li Gobbi, Mariangela Manfredi, Maria Infantino
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引用次数: 0

Abstract

The extensive research and studies conducted over the past decade have greatly improved our comprehension of the pathogenesis and risk factors associated with Spondyloarthritis (SpA). In addition, they have contributed to the advancement of novel therapeutic approaches. Although genetics still represents the primary risk factor for SpA, increasing evidence presented in this review suggests that environmental factors-such as air pollution, smoking, gut microbiota (GM), infections, and diet-also contribute to its pathogenesis. In detail, environmental particulate matters (PMs), which include ligands for the aryl hydrocarbon receptor-a cytosolic transcription factor responsive to toxic substances-facilitate the differentiation of T Helper 17 (Th17) cells, potentially exacerbating the autoinflammatory processes associated with SpA. Furthermore, smoking influences both the cellular and humoral aspects of the immune response, resulting in leukocytosis, impaired leukocyte functionality, and a decrease in various cytokines and soluble receptors, including interleukin (IL) 15, IL-1 receptor antagonist (IL-1Ra), IL-6, soluble IL-6 receptor (sIL-6R), as well as the vascular endothelial growth factor (VEGF) receptor. Studies have indicated that patients with SpA exhibit an increased prevalence of antibodies directed against a conserved epitope shared by the human leukocyte antigen B27 (HLA-B27)- and Klebsiella nitrogenase, in comparison to HLA-B27-positive controls. Additionally, current evidence regarding the GM suggests the presence of a gut-joint-skin axis, wherein the disruption of the mucosal barrier by specific bacterial species may enhance permeability to the gut-associated lymphoid tissue (GALT), resulting in localized inflammation mediated by Th1 and Th17 cells, as well as IL-17A. Finally, this review discusses the role of diet in shaping the microbial composition and its contribution to the pathogenesis of SpA. A comprehensive understanding of the mechanisms by which environmental factors influence the pathogenesis and progression of the disease could facilitate the development of novel personalized therapies targeting both external and internal environmental exposures, such as the gut microbial ecosystem.

炎性关节炎和环境:脊柱炎的原因和后果。
在过去的十年中进行了广泛的研究和研究,极大地提高了我们对脊椎关节炎(SpA)的发病机制和危险因素的理解。此外,他们还促进了新型治疗方法的发展。尽管遗传仍然是SpA的主要危险因素,但越来越多的证据表明,环境因素——如空气污染、吸烟、肠道微生物群(GM)、感染和饮食——也有助于其发病机制。具体来说,环境颗粒物(pm),包括芳烃受体的配体——一种对有毒物质有反应的细胞质转录因子——促进T辅助性17 (Th17)细胞的分化,潜在地加剧与SpA相关的自身炎症过程。此外,吸烟影响免疫反应的细胞和体液方面,导致白细胞增多,白细胞功能受损,各种细胞因子和可溶性受体减少,包括白细胞介素(IL) 15, IL-1受体拮抗剂(IL- 1ra), IL-6,可溶性IL-6受体(sIL-6R),以及血管内皮生长因子(VEGF)受体。研究表明,与HLA-B27阳性对照相比,SpA患者表现出针对人类白细胞抗原B27 (HLA-B27)和克雷伯氏菌氮酶共享的保守表位的抗体的患病率增加。此外,目前关于GM的证据表明存在肠-关节-皮肤轴,其中特定细菌物种对粘膜屏障的破坏可能增强对肠道相关淋巴组织(GALT)的渗透性,导致Th1和Th17细胞以及IL-17A介导的局部炎症。最后,本文综述了饮食在形成微生物组成中的作用及其在SpA发病机制中的作用。全面了解环境因素影响疾病发病和进展的机制,可以促进针对外部和内部环境暴露(如肠道微生物生态系统)的新型个性化治疗的发展。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Journal of Personalized Medicine
Journal of Personalized Medicine Medicine-Medicine (miscellaneous)
CiteScore
4.10
自引率
0.00%
发文量
1878
审稿时长
11 weeks
期刊介绍: Journal of Personalized Medicine (JPM; ISSN 2075-4426) is an international, open access journal aimed at bringing all aspects of personalized medicine to one platform. JPM publishes cutting edge, innovative preclinical and translational scientific research and technologies related to personalized medicine (e.g., pharmacogenomics/proteomics, systems biology). JPM recognizes that personalized medicine—the assessment of genetic, environmental and host factors that cause variability of individuals—is a challenging, transdisciplinary topic that requires discussions from a range of experts. For a comprehensive perspective of personalized medicine, JPM aims to integrate expertise from the molecular and translational sciences, therapeutics and diagnostics, as well as discussions of regulatory, social, ethical and policy aspects. We provide a forum to bring together academic and clinical researchers, biotechnology, diagnostic and pharmaceutical companies, health professionals, regulatory and ethical experts, and government and regulatory authorities.
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