Chemokine production by the BEAS-2B human bronchial epithelial cells:: Differential regulation of eotaxin, IL-8, and RANTES by TH2-and TH1-derived cytokines

被引:113
作者
Fujisawa, T
Kato, Y
Atsuta, J
Terada, A
Iguchi, K
Kamiya, H
Yamada, H
Nakajima, T
Miyamasu, M
Hirai, K
机构
[1] Mie Natl Hosp, Dept Pediat, Tsu, Mie 5140125, Japan
[2] Mie Univ, Sch Med, Dept Psychiat, Tsu, Mie 514, Japan
[3] Univ Tokyo, Sch Med, Dept Allergy & Rheumatol, Tokyo 113, Japan
[4] Univ Tokyo, Sch Med, Dept Bioregulatory Funct, Tokyo 113, Japan
关键词
chemokines; bronchial epithelial cells; eotaxin; RANTES; IFN-gamma; IL-4; IL-13; IL-8;
D O I
10.1016/S0091-6749(00)90187-8
中图分类号
R392 [医学免疫学];
学科分类号
100102 ;
摘要
Background: Bronchial epithelial cells produce many types of chemokines and may contribute to lung inflammation by recruiting inflammatory cells. The CC chemokine eotaxin is a potent, eosinophil-specific chemoattractant that has been detected in the bronchial epithelium of patients with asthma. Objectives: The aim of this study was to investigate the regulatory mechanisms of chemokine production from bronchial epithelium by inflammatory cytokines, especially T(H)2- and T(H)1-derived cytokines, in bronchial asthma. Methods: BEAS-2B human bronchial epithelial cells were cultured with TNF-alpha, IL-4, IL-13, and IFN-gamma alone or in combination, after which supernatants were assayed for eotaxin, IL-8, and RANTES proteins with ELISA. Reverse transcription-PCR was also performed. Results: TNF-alpha induced production of eotaxin, IL-8, and RANTES in a concentration-dependent manner Both IL-4 and IL-13 synergistically enhanced TNF-alpha-induced eotaxin production, whereas IL-8 plarluction induced by TNF-alpha was significantly down-regulated by the Tea-derived cytokines. IFN-gamma, a T(H)1 cytokine, counteracted the enhancing effects of IL-4 and IL-13 on eotaxin production. RANTES production by TNF-alpha was not affected by IL-4 and IL-13 but was markedly enhanced by IFN-gamma. Conclusions:These results suggest that T(H)2 cytokines are involved in preferential recruitment of eosinophils in bronchial asthma by enhancing eotaxin and reducing IL-8 production from bronchial epithelial cells and that T(H)1 cytokines counteract the effects of T(H)2 cytokines by reducing eotaxin production.
引用
收藏
页码:126 / 133
页数:8
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