Mashikian M V, Tarpy R E, Saukkonen J J, Lim K G, Fine G D, Cruikshank W W, Center D M
Pulmonary Center, Boston University School of Medicine, Mass, USA.
J Allergy Clin Immunol. 1998 Jun;101(6 Pt 1):786-92. doi: 10.1016/s0091-6749(98)70403-8.
We have previously demonstrated that the earliest lymphocyte chemotactic factors present in bronchoalveolar lavage fluid (BALF) of subjects with atopic asthma after subsegmental antigen challenge are IL-16 and MIP-1alpha, of which IL-16 appears to contribute a majority of the chemotactic activity. Because IL-16 is released in vitro after histamine stimulation of CD8+ T cells and epithelial cells, we evaluated the potential role of histamine in the release of IL-16 into the airways of allergic asthmatics in vivo.
Eight allergic asthmatic subjects, six normal subjects, and six atopic nonasthmatic subjects were challenged with saline in the lingula and with serial concentrations of histamine (1 x 10(-7) to 5 x 10(-5) mol/L) in the right middle lobe followed by bronchoalveolar lavage (BAL) 15 minutes and 6 hours later.
The BALF from saline- and histamine-challenged lobes of normal subjects and atopic nonasthmatic subjects contained no significant lymphocyte chemoattractant activity. In six of the eight atopic asthmatic subjects, the histamine-challenged but not saline-challenged segment contained IL-16 chemotactic activity but no other identifiable lymphocyte chemoattractant activities at 6 hours.
IL-16 appears in the airways after histamine challenge and therefore could contribute to the earliest infiltration of CD4+ T cells and eosinophils observed after antigen challenge due to histamine release from mast cells.
我们之前已经证明,在变应性哮喘患者亚段抗原激发后支气管肺泡灌洗液(BALF)中最早出现的淋巴细胞趋化因子是IL-16和MIP-1α,其中IL-16似乎贡献了大部分趋化活性。由于IL-16在组胺刺激CD8⁺T细胞和上皮细胞后在体外释放,我们评估了组胺在体内将IL-16释放到变应性哮喘患者气道中的潜在作用。
8名变应性哮喘患者、6名正常受试者和6名变应性非哮喘受试者,舌叶用盐水激发,右中叶用系列浓度的组胺(1×10⁻⁷至5×10⁻⁵mol/L)激发,随后在15分钟和6小时后进行支气管肺泡灌洗(BAL)。
正常受试者和变应性非哮喘受试者盐水和组胺激发叶的BALF中没有显著的淋巴细胞趋化活性。在8名变应性哮喘患者中的6名中,组胺激发而非盐水激发的节段在6小时时含有IL-16趋化活性,但没有其他可识别的淋巴细胞趋化活性。
组胺激发后气道中出现IL-16,因此可能导致抗原激发后最早观察到的CD4⁺T细胞和嗜酸性粒细胞浸润,这是由于肥大细胞释放组胺所致。