免疫系统
肺泡巨噬细胞
发病机制
机制(生物学)
病态的
肺毒性
免疫学
硫芥
医学
免疫病理学
炎症
肺
巨噬细胞
病理
毒性
生物
体外
遗传学
内科学
哲学
认识论
作者
Somayeh Sadeghi,Mahtab Tapak,Tooba Ghazanfari,Nariman Mosaffa
标识
DOI:10.1016/j.toxlet.2020.07.035
摘要
Despite many studies investigating the mechanism of Sulfur Mustard (SM) induced lung injury, the underlying mechanism is still unclear. Inflammatory and subsequent fibroproliferative stages of SM-toxicity are based upon several highly-related series of events controlled by the immune system. The inhalation of SM gas variably affects different cell populations within the lungs. Various studies have shown the critical role of macrophages in triggering a pulmonary inflammatory response as well as its maintenance, resolution, and repair. Importantly, macrophages can serve as either pro-inflammatory or anti-inflammatory populations depending on the present conditions at any pathological stage. Different characteristics of macrophages, including their differentiation, phenotypic, and functional properties, as well as interactions with other cell populations determine the outcomes of lung diseases and the extent of long- or short-term pulmonary damage induced by SM. In this paper, we summarize the current state of knowledge regarding the role of alveolar macrophages and their mediators in the pathogenesis of SM in pulmonary injury. Investigating the specific cells and mechanisms involved in SM-lung injury may be useful in finding new target opportunities for treatment of this injury.
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