Silva Juliana da Costa, Thompson-Souza Glaucia de Azevedo, Barroso Marina Valente, Neves Josiane Sabbadini, Figueiredo Rodrigo Tinoco
Institute of Microbiology Paulo de Góes, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil.
Institute of Biomedical Sciences, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil.
Front Microbiol. 2021 Feb 18;12:634043. doi: 10.3389/fmicb.2021.634043. eCollection 2021.
Fungal infections represent a worldwide health problem. Fungal pathogens are responsible for a variety of conditions, including superficial diseases, allergic pathologies and potentially lethal invasive infections. Neutrophils and eosinophils have been implicated as effector cells in several pathologies. Neutrophils are major effector cells involved in the control of fungal infections and exhibit a plethora of antifungal mechanisms, such as phagocytosis, reactive oxygen species production, degranulation, extracellular vesicle formation, and DNA extracellular trap (ET) release. Eosinophils are polymorphonuclear cells classically implicated as effector cells in the pathogenesis of allergic diseases and helminthic infections, although their roles as immunomodulatory players in both innate and adaptive immunity are currently recognized. Eosinophils are also endowed with antifungal activities and are abundantly found in allergic conditions associated with fungal colonization and sensitization. Neutrophils and eosinophils have been demonstrated to release their nuclear and mitochondrial DNA in response to many pathogens and pro-inflammatory stimuli. ETs have been implicated in the killing and control of many pathogens, as well as in promoting inflammation and tissue damage. The formation of ETs by neutrophils and eosinophils has been described in response to pathogenic fungi. Here, we provide an overview of the mechanisms involved in the release of neutrophil and eosinophil ETs in response to fungal pathogens. General implications for understanding the formation of ETs and the roles of ETs in fungal infections are discussed.
真菌感染是一个全球性的健康问题。真菌病原体可导致多种病症，包括浅表疾病、过敏性疾病以及可能致命的侵袭性感染。中性粒细胞和嗜酸性粒细胞在多种病症中被认为是效应细胞。中性粒细胞是参与控制真菌感染的主要效应细胞，并展现出大量抗真菌机制，如吞噬作用、活性氧生成、脱颗粒、细胞外囊泡形成以及细胞外DNA陷阱（ET）释放。嗜酸性粒细胞是多形核细胞，传统上被认为是过敏性疾病和蠕虫感染发病机制中的效应细胞，尽管目前人们已认识到它们在固有免疫和适应性免疫中作为免疫调节参与者的作用。嗜酸性粒细胞也具有抗真菌活性，并且在与真菌定植和致敏相关的过敏性疾病中大量存在。中性粒细胞和嗜酸性粒细胞已被证明会响应多种病原体和促炎刺激而释放其核DNA和线粒体DNA。ETs与许多病原体的杀伤和控制有关，也与促进炎症和组织损伤有关。已有研究描述了中性粒细胞和嗜酸性粒细胞针对致病性真菌形成ETs的情况。在此，我们概述了中性粒细胞和嗜酸性粒细胞响应真菌病原体释放ETs所涉及的机制。讨论了理解ETs形成及其在真菌感染中的作用的一般意义。
