Elevated soluble ADAM8 in bronchoalveolar lavage fluid in patients with eosinophilic pneumonia

被引:32
作者
Matsuno, Osamu
Miyazaki, Eishi
Nureki, Shinichi
Ueno, Takuya
Ando, Masaru
Ito, Kazunobu
Kumamoto, Toshihide
Higuchi, Yasunori
机构
[1] Oita Univ, Fac Med, Dept Brain & Nerve Sci, Div Resp Dis, Yufu, Oita 8795593, Japan
[2] Oita Univ, Fac Med, Res Ctr Appl Med Engn, Yufu, Oita 8795593, Japan
[3] Shin Beppu Hosp, Beppu, Oita, Japan
关键词
ADAM8; VCAM-1; CD23; eosinophilic pneumonia;
D O I
10.1159/000097359
中图分类号
R392 [医学免疫学];
学科分类号
100102 ;
摘要
Background: ADAM (a disintegrin and metalloprotease) family members, characterized by a metalloprotease and a disintegrin domain, are membrane-anchored glycoproteins involved in proteolysis and cell adhesion. ADAM8 might have an important role in allergic inflammation. It can cleave a variety of substrates and is a sheddase for VCAM-1 and CD23, the low-affinity IgE receptors. Methods: To evaluate the contribution of ADAM8 to the pathogenesis of eosinophilic pneumonia (EP), we measured the concentrations of soluble ADAM8 (sADAM8) and its substrates, soluble VCAM-1 (sVCAM-1) and soluble CD23 (sCD23), in bronchoalveolar lavage fluid from patients with smoking-induced acute eosinophilic pneumonia (AEP), chronic idiopathic eosinophilic pneumonia (CEP), and drug-induced eosinophilic pneumonia (drug-EP). Results: The sADAM8 and sVCAM-1 concentrations were increased in AEP and CEP. The sCD23 concentration was elevated in AEP. In AEP, but not CEP, the sADAM8 concentration significantly correlated with those of both sVCAM and sCD23. Conclusion: The pathogenesis of AEP, CEP, and drug-EP was distinct with regard to ADAM8. Our results are the first to associate ADAM8 with eosinophilic responses and lung inflammation in humans. Copyright (c) 2007 S. Karger AG, Basel.
引用
收藏
页码:285 / 290
页数:6
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