Nagata Makoto, Saito Keiko, Tsuchiya Koji, Sakamoto Yoshio
Pulmonary Division, Second Department of Internal Medicine, Saitama Medical School.
J Allergy Clin Immunol. 2002 Apr;109(4):676-80. doi: 10.1067/mai.2002.122841.
Eosinophils (EOS) are one of the cellular sources of cysteinyl leukotrienes (cysLTs) in allergic inflammation. There is evidence that cysLT(1)receptor antagonists possess anti-inflammatory properties in vivo in asthmatic airways. Although the exact mechanism of action remains unknown, cysLTs might regulate the cellular responses involved in allergic inflammation.
The present study was undertaken to examine whether LTD(4)modifies the adhesive property of EOS.
EOS were isolated from the blood of healthy subjects. Their adhesion to tissue culture plates or recombinant human (rh) adhesion proteins was then examined in the presence or absence of LTD(4).
LTD(4)significantly augmented EOS adhesion to tissue culture plates (adhesion: 5.0% +/- 0.5% by medium control vs 9.1% +/- 1.2% by 1 micromol/L; P <.01; n = 10). The enhanced adhesion induced by LTD(4) was blocked by pranlukast, a cysLT(1) receptor antagonist, or an anti-beta(2) integrin antibody. Flow cytometry analysis revealed that LTD(4) significantly enhanced the expression of CD11b and CD18 on the EOS surface. Finally, LTD(4) augmented EOS adhesion to rh intercellular cell adhesion molecule 1 but not to rh vascular cell adhesion molecule 1 or fibronectin.
The results suggest that LTD(4) directly upregulates the adhesive property of EOS via the cysLT(1) receptor and beta(2) integrin. LTD(4) generated from EOS or cells of some other type might contribute to the development of phenotypic change in airway EOS.
嗜酸性粒细胞（EOS）是变应性炎症中半胱氨酰白三烯（cysLTs）的细胞来源之一。有证据表明，cysLT（1）受体拮抗剂在哮喘气道体内具有抗炎特性。尽管确切的作用机制尚不清楚，但cysLTs可能调节变应性炎症中涉及的细胞反应。
本研究旨在探讨白三烯D4（LTD4）是否改变EOS的黏附特性。
从健康受试者血液中分离出EOS。然后在有或无LTD4存在的情况下，检测它们对组织培养板或重组人（rh）黏附蛋白的黏附情况。
LTD4显著增强EOS对组织培养板的黏附（黏附率：培养基对照组为5.0%±0.5%，1 μmol/L LTD4组为9.1%±1.2%；P<0.01；n = 10）。LTD4诱导的黏附增强被cysLT（1）受体拮抗剂普仑司特或抗β（2）整合素抗体阻断。流式细胞术分析显示，LTD4显著增强EOS表面CD11b和CD18的表达。最后，LTD4增强EOS对rh细胞间黏附分子1的黏附，但对rh血管细胞黏附分子1或纤连蛋白无此作用。
结果表明，LTD4通过cysLT（1）受体和β（2）整合素直接上调EOS的黏附特性。由EOS或其他某些类型细胞产生的LTD4可能有助于气道EOS表型变化的发生。
