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首页> 美国卫生研究院文献>American Journal of Physiology - Lung Cellular and Molecular Physiology >Translational Research in Acute Lung Injury and Pulmonary Fibrosis: Alcohol abuse and smoking alter inflammatory mediator production by pulmonary and systemic immune cells
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Translational Research in Acute Lung Injury and Pulmonary Fibrosis: Alcohol abuse and smoking alter inflammatory mediator production by pulmonary and systemic immune cells

机译：急性肺损伤和肺纤维化的转化研究：酗酒和吸烟改变肺和全身免疫细胞的炎症介质产生

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Alcohol use disorders (AUDs) and tobacco smoking are associated with an increased predisposition for community-acquired pneumonia and the acute respiratory distress syndrome. Mechanisms are incompletely established but may include alterations in response to pathogens by immune cells, including alveolar macrophages (AMs) and peripheral blood mononuclear cells (PBMCs). We sought to determine the relationship of AUDs and smoking to expression of IFNγ, IL-1β, IL-6, and TNFα by AMs and PBMCs from human subjects after stimulation with lipopolysaccharide (LPS) or lipoteichoic acid (LTA). AMs and PBMCs from healthy subjects with AUDs and controls, matched on smoking, were cultured with LPS (1 μg/ml) or LTA (5 μg/ml) in the presence and absence of the antioxidant precursor N-acetylcysteine (10 mM). Cytokines were measured in cell culture supernatants. Expression of IFNγ, IL-1β, IL-6, and TNFα in AMs and PBMCs was significantly increased in response to stimulation with LPS and LTA. AUDs were associated with augmented production of proinflammatory cytokines, particularly IFNγ and IL-1β, by AMs and PBMCs in response to LPS. Smoking diminished the impact of AUDs on AM cytokine expression. Expression of basal AM and PBMC Toll-like receptors-2 and -4 was not clearly related to differences in cytokine expression; however, addition of N-acetylcysteine with LPS or LTA led to diminished AM and PBMC cytokine secretion, especially among current smokers. Our findings suggest that AM and PBMC immune cell responses to LPS and LTA are influenced by AUDs and smoking through mechanisms that may include alterations in cellular oxidative stress.
机译：饮酒障碍（AUDs）和吸烟与社区获得性肺炎和急性呼吸窘迫综合征的易感性增加有关。机制尚未完全确立，但可能包括免疫细胞对病原体的反应发生改变，包括肺泡巨噬细胞（AM）和外周血单核细胞（PBMC）。我们试图确定脂多糖（LPS）或脂蛋白酸（LTA）刺激后，来自人类受试者的AMs和PBMC，AUD和吸烟与IFNγ，IL-1β，IL-6和TNFα的表达之间的关系。在存在和不存在抗氧化剂前体N-乙酰半胱氨酸（10 mM）的情况下，将LPS（1μg/ ml）或LTA（5μg/ ml）培养得来的，具有AUD和对照的健康受试者的AMs和PBMCs与吸烟匹配。在细胞培养上清液中测量细胞因子。 LPS和LTA刺激后，AMs和PBMC中IFNγ，IL-1β，IL-6和TNFα的表达显着增加。 AUD与AM和PBMC响应LPS增加促炎细胞因子，特别是IFNγ和IL-1β的产生有关。吸烟减少了AUDs对AM细胞因子表达的影响。基底性AM和PBMC Toll样受体2和-4的表达与细胞因子表达的差异没有明显关系。然而，在LPS或LTA中加入N-乙酰半胱氨酸会导致AM和PBMC细胞因子分泌减少，特别是在目前的吸烟者中。我们的发现表明AM和PBMC对LPS和LTA的免疫细胞反应受AUD和吸烟的影响，其机制可能包括细胞氧化应激的改变。

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