Nureki Shin-ichi, Miyazaki Eishi, Ando Masaru, Kumamoto Toshihide, Tsuda Tomiyasu
Division of Pulmonary Disease, Third Department of Internal Medicine, Oita University Faculty of Medicine, 1-1 Idaigaoka, Hasama-machi, Oita 879-5593, Japan.
Clin Immunol. 2005 Jul;116(1):83-93. doi: 10.1016/j.clim.2005.03.001.
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.
我们检测了香烟烟雾相关性急性嗜酸性粒细胞性肺炎（CS-AEP）患者支气管肺泡灌洗液（BALF）细胞中巨噬细胞源性趋化因子（MDC/CCL22）和胸腺激活调节趋化因子（TARC/CCL17）的产生情况。CS-AEP患者BALF中CC趋化因子受体4（CCR4）配体水平显著高于健康志愿者，且与Th2细胞因子水平密切相关。白细胞介素-4可增强CCR4配体的产生。在CS-AEP患者及健康对照吸烟者的CD68阳性细胞中均观察到MDC表达。相比之下，仅在CS-AEP患者中检测到CD68或CD1a阳性细胞中有TARC表达。体内香烟烟雾激发试验导致BALF及BALF贴壁细胞培养上清液中CCR4配体增加。这些结果表明，肺泡巨噬细胞和树突状细胞可能通过产生CCR4配体（可能是对香烟烟雾的反应）参与CS-AEP的发病机制。
