Katoh S, Matsumoto N, Fukushima K, Mukae H, Kadota J I, Kohno S, Matsukura S
Third Department of Internal Medicine, Miyazaki Medical College, Miyazaki, Japan.
J Allergy Clin Immunol. 2000 Oct;106(4):730-6. doi: 10.1067/mai.2000.109827.
Allergic lung inflammation is caused by accumulation and activation of different leukocyte subsets, such as eosinophils and T lymphocytes, in the lung. The chemokines are a large group of chemotactic cytokines that regulate leukocyte trafficking and may play an important role in allergic lung inflammation.
The purpose of this study was to evaluate the role of various chemokines, including eotaxin, RANTES, monocyte chemotactic protein (MCP)-1, macrophage inflammatory protein (MIP)-1beta, and IL-8 in the pathogenesis of eosinophilic pneumonia (EP).
The concentrations of eotaxin, RANTES, MCP-1, MIP-1beta, and IL-8 in bronchoalveolar lavage fluid (BALF) were measured by using ELISA in 15 patients with EP, 10 with idiopathic pulmonary fibrosis, 10 with sarcoidosis, and 11 healthy volunteers.
Eotaxin in BALF was high only in patients with EP, and its level correlated significantly with the number of eosinophils in BALF of patients with EP and healthy volunteers. MCP-1 and MIP-1beta in BALF were preferentially increased in patients with EP. There was a significant correlation between MCP-1 levels and the number of macrophages in BALF of patients with EP and healthy volunteers.
Our findings suggest that these CC chemokines contribute to the pathogenesis of EP through the specific recruitment of leukocyte subsets in the lung.
过敏性肺部炎症是由肺部不同白细胞亚群(如嗜酸性粒细胞和T淋巴细胞)的积聚和激活引起的。趋化因子是一大类趋化性细胞因子,可调节白细胞的迁移,可能在过敏性肺部炎症中起重要作用。
本研究旨在评估包括嗜酸性粒细胞趋化因子、调节激活正常T细胞表达和分泌的因子(RANTES)、单核细胞趋化蛋白(MCP)-1、巨噬细胞炎性蛋白(MIP)-1β和白细胞介素(IL)-8在内的多种趋化因子在嗜酸性粒细胞性肺炎(EP)发病机制中的作用。
采用酶联免疫吸附测定法(ELISA)检测15例EP患者、10例特发性肺纤维化患者、10例结节病患者和11名健康志愿者支气管肺泡灌洗液(BALF)中嗜酸性粒细胞趋化因子、RANTES、MCP-1、MIP-1β和IL-8的浓度。
仅EP患者的BALF中嗜酸性粒细胞趋化因子水平较高,其水平与EP患者及健康志愿者BALF中嗜酸性粒细胞数量显著相关。EP患者BALF中的MCP-1和MIP-1β优先升高。EP患者及健康志愿者BALF中MCP-1水平与巨噬细胞数量之间存在显著相关性。
我们的研究结果表明,这些CC趋化因子通过在肺中特异性募集白细胞亚群而促进EP的发病机制。