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从生物多样性和表观遗传变化的角度理解哮喘和过敏

Understanding Asthma and Allergies by the Lens of Biodiversity and Epigenetic Changes.

机构信息

Instituto de Ciências da Saúde, Universidade Federal da Bahia, Salvador, Brazil.

Instituto de Biologia, Universidade Federal da Bahia, Salvador, Brazil.

出版信息

Front Immunol. 2021 Mar 1;12:623737. doi: 10.3389/fimmu.2021.623737. eCollection 2021.

Abstract

Exposure to different organisms (bacteria, mold, virus, protozoan, helminths, among others) can induce epigenetic changes affecting the modulation of immune responses and consequently increasing the susceptibility to inflammatory diseases. Epigenomic regulatory features are highly affected during embryonic development and are responsible for the expression or repression of different genes associated with cell development and targeting/conducting immune responses. The well-known, "window of opportunity" that includes maternal and post-natal environmental exposures, which include maternal infections, microbiota, diet, drugs, and pollutant exposures are of fundamental importance to immune modulation and these events are almost always accompanied by epigenetic changes. Recently, it has been shown that these alterations could be involved in both risk and protection of allergic diseases through mechanisms, such as DNA methylation and histone modifications, which can enhance Th2 responses and maintain memory Th2 cells or decrease Treg cells differentiation. In addition, epigenetic changes may differ according to the microbial agent involved and may even influence different asthma or allergy phenotypes. In this review, we discuss how exposure to different organisms, including bacteria, viruses, and helminths can lead to epigenetic modulations and how this correlates with allergic diseases considering different genetic backgrounds of several ancestral populations.

摘要

暴露于不同的生物体(细菌、霉菌、病毒、原生动物、寄生虫等)会引起表观遗传变化,影响免疫反应的调节,从而增加患炎症性疾病的易感性。在胚胎发育过程中,表观基因组调控特征受到高度影响,负责不同基因的表达或抑制,这些基因与细胞发育和靶向/进行免疫反应有关。众所周知,包括母体和产后环境暴露的“机会之窗”,包括母体感染、微生物群、饮食、药物和污染物暴露,对免疫调节至关重要,这些事件几乎总是伴随着表观遗传变化。最近,已经表明这些改变可能通过 DNA 甲基化和组蛋白修饰等机制参与过敏疾病的风险和保护,这些机制可以增强 Th2 反应并维持记忆性 Th2 细胞或减少 Treg 细胞分化。此外,表观遗传变化可能因涉及的微生物剂而异,甚至可能影响不同的哮喘或过敏表型。在这篇综述中,我们讨论了暴露于不同的生物体,包括细菌、病毒和寄生虫,如何导致表观遗传调节,以及考虑到几个祖先进化群体的不同遗传背景,这与过敏疾病有何关联。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/706b/7957070/8da0c5e9b505/fimmu-12-623737-g0001.jpg

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