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首页> 外文期刊>Toxicology: An International Journal Concerned with the Effects of Chemicals on Living Systems >In vivo hydroquinone exposure impairs MCP-1 secretion and monocyte recruitment into the inflamed lung
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In vivo hydroquinone exposure impairs MCP-1 secretion and monocyte recruitment into the inflamed lung

机译：体内对苯二酚暴露会损害MCP-1分泌并将单核细胞募集入发炎的肺

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摘要

Alveolar macrophages (AMs) are important cells in the resolution of the inflammatory process and they come into direct contact with inhaled pollutants. Hydroquinone (HQ) is an environmental pollutant and a component of cigarette smoke that causes immunosuppressive effects. In the present work, we showed that mice exposed to low levels of aerosolized HQ (25. ppm; 1. h/day/5 days) presented impaired mononuclear cell migration to the lipopolysaccharide (LPS)-inflamed lung. This may have been due to reduced monocyte chemoattractant protein-1 (MCP-1) secretion into bronchoalveolar lavage fluid (BALF), and it was not related to alterations to mononuclear cell mobilization into the blood or adhesion molecules expression on mononuclear cell membranes. Corroborating the actions of HQ on MCP-1 secretion, reduced MCP-1 concentrations were also found in the supernatant of . ex vivo AM and tracheal tissue collected from HQ-exposed mice. A direct action of HQ on MCP-1 secretion, resulting from impaired gene synthesis, was verified by . in vitro incubation of naive AMs or tracheal tissue with HQ. The role of reduced levels of MCP-1 in the BALF on monocyte migration was analysed in the human monocytic lineage THP-1 in . in vitro chemotaxis assays, which showed that the reduced concentrations of MCP-1 found in the BALF or cell supernatants from HQ-exposed mice impaired cell migration. Considering the fact that MCP-1 presents a broad spectrum of actions on pathophysiological conditions and that resident mononuclear cells are involved in lung tissue homeostasis and in immune host defence, the mechanism of HQ toxicity presented herein might be relevant to the genesis of infectious lung diseases in smokers and in inhabitants of polluted areas.
机译：肺泡巨噬细胞（AMs）是解决炎症过程的重要细胞，它们与吸入的污染物直接接触。对苯二酚（HQ）是一种环境污染物，是香烟烟雾中引起免疫抑制作用的成分。在当前的工作中，我们显示了暴露于低水平的雾化HQ（25. ppm; 1. h / day / 5天）的小鼠单核细胞迁移到脂多糖（LPS）刺激的肺中受损。这可能是由于单核细胞趋化蛋白1（MCP-1）分泌到支气管肺泡灌洗液（BALF）中减少，并且与单核细胞动员到血液中的变化或单核细胞膜上粘附分子表达的改变无关。证实HQ对MCP-1分泌的作用，还发现MCP-1的上清液中MCP-1浓度降低。从暴露于HQ的小鼠体内提取AM和气管组织。 HQ对基因合成受损导致的HQ对MCP-1分泌的直接作用进行了验证。将未成熟的AM或气管组织与HQ进行体外培养。在人类单核细胞系THP-1中分析了BALF中MCP-1水平降低对单核细胞迁移的作用。体外趋化性试验表明，BALF或HQ暴露小鼠的细胞上清液中MCP-1浓度降低，从而损害了细胞迁移。考虑到MCP-1在病理生理条件下表现出广泛的作用并且驻留的单核细胞参与肺组织动态平衡和免疫宿主防御这一事实，本文提出的HQ毒性机制可能与传染性肺病的发生有关在吸烟者和污染地区的居民中。

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