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挥发性有机化合物:自身免疫性疾病中的促炎激活物。

Volatile organic compounds: A proinflammatory activator in autoimmune diseases.

机构信息

Department of Science Laboratory Technology, University of Nigeria, Nsukkagu, Enugu State, Nigeria.

Department of Plant Science and Biotechnology, University of Nigeria, Nsukka, Enugu State, Nigeria.

出版信息

Front Immunol. 2022 Jul 29;13:928379. doi: 10.3389/fimmu.2022.928379. eCollection 2022.

DOI:10.3389/fimmu.2022.928379
PMID:35967306
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9373925/
Abstract

The etiopathogenesis of inflammatory and autoimmune diseases, including pulmonary disease, atherosclerosis, and rheumatoid arthritis, has been linked to human exposure to volatile organic compounds (VOC) present in the environment. Chronic inflammation due to immune breakdown and malfunctioning of the immune system has been projected to play a major role in the initiation and progression of autoimmune disorders. Macrophages, major phagocytes involved in the regulation of chronic inflammation, are a major target of VOC. Excessive and prolonged activation of immune cells (T and B lymphocytes) and overexpression of the master pro-inflammatory constituents [cytokine and tumor necrosis factor-alpha, together with other mediators (interleukin-6, interleukin-1, and interferon-gamma)] have been shown to play a central role in the pathogenesis of autoimmune inflammatory responses. The function and efficiency of the immune system resulting in immunostimulation and immunosuppression are a result of exogenous and endogenous factors. An autoimmune disorder is a by-product of the overproduction of these inflammatory mediators. Additionally, an excess of these toxicants helps in promoting autoimmunity through alterations in DNA methylation in CD4 T cells. The purpose of this review is to shed light on the possible role of VOC exposure in the onset and progression of autoimmune diseases.

摘要

炎症和自身免疫性疾病(包括肺部疾病、动脉粥样硬化和类风湿性关节炎)的病因与人类暴露于环境中存在的挥发性有机化合物(VOC)有关。由于免疫系统的免疫破坏和功能障碍而导致的慢性炎症,预计在自身免疫性疾病的发生和进展中发挥主要作用。巨噬细胞是参与慢性炎症调节的主要吞噬细胞,是 VOC 的主要靶标。过度和持续激活免疫细胞(T 和 B 淋巴细胞)以及主前炎症成分[细胞因子和肿瘤坏死因子-α,以及其他介质(白细胞介素-6、白细胞介素-1 和干扰素-γ)]的过度表达,在自身免疫性炎症反应的发病机制中发挥着核心作用。导致免疫刺激和免疫抑制的免疫系统的功能和效率是外源性和内源性因素的结果。自身免疫性疾病是这些炎症介质过度产生的副产品。此外,这些有毒物质的过量通过改变 CD4 T 细胞中的 DNA 甲基化有助于促进自身免疫。本综述的目的是阐明 VOC 暴露在自身免疫性疾病的发生和进展中的可能作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dee0/9373925/2f1bb492f503/fimmu-13-928379-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dee0/9373925/0c35e31bb03e/fimmu-13-928379-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dee0/9373925/611c01512423/fimmu-13-928379-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dee0/9373925/02bc18f56d3c/fimmu-13-928379-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dee0/9373925/2f1bb492f503/fimmu-13-928379-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dee0/9373925/0c35e31bb03e/fimmu-13-928379-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dee0/9373925/611c01512423/fimmu-13-928379-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dee0/9373925/02bc18f56d3c/fimmu-13-928379-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dee0/9373925/2f1bb492f503/fimmu-13-928379-g004.jpg

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