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抗原激发哮喘患者支气管肺泡灌洗液中白细胞介素-16(淋巴细胞趋化因子)和巨噬细胞炎性蛋白1α(MIP1α)的早期鉴定。

Early identification of interleukin-16 (lymphocyte chemoattractant factor) and macrophage inflammatory protein 1 alpha (MIP1 alpha) in bronchoalveolar lavage fluid of antigen-challenged asthmatics.

作者信息

Cruikshank W W, Long A, Tarpy R E, Kornfeld H, Carroll M P, Teran L, Holgate S T, Center D M

机构信息

Pulmonary Center, Boston University School of Medicine, Massachusetts, USA.

出版信息

Am J Respir Cell Mol Biol. 1995 Dec;13(6):738-47. doi: 10.1165/ajrcmb.13.6.7576712.

DOI:10.1165/ajrcmb.13.6.7576712
PMID:7576712
Abstract

Accumulation of CD4+ interleukin (IL)-2R+ lymphocytes in the airways of asthmatics is generally attributed to the presence of chemoattractant cytokines. The precise mechanism for the initiation of the earliest CD4+ lymphocyte infiltration and activation is unknown. In this study, we describe for the first time the presence of lymphocyte chemoattractant activity in the bronchoalveolar lavage (BAL) fluid obtained from asthmatics 6 h after antigen challenge. The majority of the chemoattractant activity at this early time point is represented by IL-16 (lymphocyte chemoattractant factor), a CD4+ cell-specific chemoattractant and growth factor. In addition to IL-16, macrophage inflammatory protein 1 alpha (MIP1 alpha) chemotactic bioactivity was detected in significant levels. While IL-16, MIP1 alpha, and IL-8 were all identified by enzyme-linked immunosorbent assay, the great majority of the lymphocyte chemoattractant activity in the BAL fluid after antigen challenge is attributable to IL-16 and MIP1 alpha. There were no detectable levels of IL-16 nor MIP1 alpha in BAL fluid of antigen-challenged normal subjects nor atopic nonasthmatics nor in saline-challenged lobes from the asthmatics. The identification of multiple lymphocyte chemoattractants early after antigen challenge suggests a complex cellular, as well as chemoattractant cytokine, profile in initiating the CD4+ T cell-mediated inflammatory process that is specific for the atopic asthmatic phenotype.

摘要

哮喘患者气道中CD4 + 白细胞介素(IL)-2R + 淋巴细胞的积聚通常归因于趋化因子细胞因子的存在。最早的CD4 + 淋巴细胞浸润和激活起始的确切机制尚不清楚。在本研究中,我们首次描述了抗原激发6小时后从哮喘患者获得的支气管肺泡灌洗(BAL)液中存在淋巴细胞趋化活性。在这个早期时间点,大多数趋化活性由IL-16(淋巴细胞趋化因子)代表,IL-16是一种CD4 + 细胞特异性趋化因子和生长因子。除IL-16外,还检测到显著水平的巨噬细胞炎性蛋白1α(MIP1α)趋化生物活性。虽然通过酶联免疫吸附测定法鉴定了IL-16、MIP1α和IL-8,但抗原激发后BAL液中绝大多数淋巴细胞趋化活性归因于IL-16和MIP1α。在抗原激发的正常受试者、特应性非哮喘患者的BAL液中以及哮喘患者盐水激发的肺叶中均未检测到IL-16和MIP1α水平。抗原激发后早期多种淋巴细胞趋化因子的鉴定表明,在启动特应性哮喘表型特有的CD4 + T细胞介导的炎症过程中,存在复杂的细胞以及趋化因子细胞因子谱。

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