Bradykinin stimulates type II alveolar cells to release neutrophil and monocyte chemotactic activity and inflammatory cytokines

被引:44
作者
Koyama, S
Sato, E
Nomura, H
Kubo, K
Miura, M
Yamashita, T
Nagai, S
Izumi, T
机构
[1] Shinshu Univ, Sch Med, Dept Internal Med 1, Matsumoto, Nagano 390, Japan
[2] Mitsubishi Kagaku BCL, Tokyo, Japan
[3] Kyoto Univ, Chest Dis Res Inst, Kyoto 606, Japan
关键词
D O I
10.1016/S0002-9440(10)65702-1
中图分类号
R36 [病理学];
学科分类号
100104 ;
摘要
In the present study, we evaluated the potential of bradykinin (BK) to induce the release of neutrophil and monocyte chemotactic activity (NCA and MCA) and cytokines from an alveolar type II epithelial cell line, A549 cells. BK stimulated A549 cells to release NCI and MCA in a dose- and time-dependent manner (P < 0.001), Checkerboard analysis revealed that both NCA and MCA involved chemotactic and chemokinetic activity. Molecular sieve column chromatography showed three molecular weight masses (near 19 kd, 8 kd, and 400 d) for NCA and several molecular weight peaks (near 66 kd, 25 kd, 19 kd, 16 kd, and 400 d) for MCA. The release of NCA and MCA was inhibited by cycloheximide and lipoxygenase inhibitors (P < 0.01), The NCA and MCA were inhibited by leukotriene B4 (LTB4) receptor antagonist(P < 0.01), and the concentration of LTB4 was high enough for NCA and MCA, Antibodies to interleukin (IL)-8 and granulocyte colony-stimulating factor (G-CSF) attenuated NCA (P < 0.01), and antibodies to monocyte chemotactic protein-1 (MCP-1), G-CSF, and transforming growth factor (TGF)-beta attenuated MCA (P < 0.01), The levels of IL-8, G-CSF, MCP-1, and TGF-beta increased time dependently(P < 0.01), BK also stimulated the release of ILeukin-6 from A543 cells (P < 0.001). The receptors responsible for the release of NCA, MCA, and individual chemokines involved both BKB1 and BKB2 receptors, These data suggest that BK may stimulate alveolar type II pneumocytes to release inflammatory cytokines, which then may modulate the lung inflammation.
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收藏
页码:1885 / 1893
页数:9
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