首页> 外文期刊>Clinical immunology: The official journal of the Clinical Immunology Society >CC chemokine receptor 4 ligand production by bronchoalveolar lavage fluid cells in cigarette-smoke-associated acute eosinophilic pneumonia.
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CC chemokine receptor 4 ligand production by bronchoalveolar lavage fluid cells in cigarette-smoke-associated acute eosinophilic pneumonia.

机译:支气管肺泡灌洗液细胞在香烟烟雾相关的急性嗜酸性粒细胞性肺炎中产生CC趋化因子受体4配体。

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摘要

We examined the production of macrophage-derived chemokine (MDC/CCL22) and thymus- and activation-regulated chemokine (TARC/CCL17) by bronchoalveolar lavage fluid (BALF) cells in cigarette-smoke-associated acute eosinophilic pneumonia (CS-AEP). The CC Chemokine Receptor 4 (CCR4) ligand levels in BALF from patients with CS-AEP were considerably higher than those in healthy volunteers and correlated well with Th2 cytokine levels. Interleukin-4 enhanced CCR4 ligand production. MDC expression was observed in CD68-positive cells from patients with CS-AEP and in healthy control smokers. In contrast, TARC expression in CD68- or CD1a-positive cells was detected only in CS-AEP. An in vivo cigarette smoke challenge test induced increases in CCR4 ligands in the BALF and in the cultured supernatant of BALF adherent cells. These results suggest that alveolar macrophages and dendritic cells contribute to the pathogenesis of CS-AEP by generating CCR4 ligands, probably in response to cigarette smoke.
机译:我们检查了支气管肺泡灌洗液(BALF)细胞在香烟烟相关的急性嗜酸性粒细胞性肺炎(CS-AEP)中产生巨噬细胞衍生的趋化因子(MDC / CCL22)和胸腺和活化调节的趋化因子(TARC / CCL17)。 CS-AEP患者的BALF中CC趋化因子受体4(CCR4)配体水平显着高于健康志愿者,并且与Th2细胞因子水平相关。白介素4增强CCR4配体的生产。在CS-AEP患者和健康对照吸烟者的CD68阳性细胞中观察到MDC表达。相反,仅在CS-AEP中检测到CD68或CD1a阳性细胞中的TARC表达。体内香烟烟雾攻击测试诱导了BALF和BALF贴壁细胞培养上清液中CCR4配体的增加。这些结果表明,肺泡巨噬细胞和树突状细胞可能通过响应香烟烟雾,通过产生CCR4配体来促进CS-AEP的发病。

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