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体内给予粒细胞-巨噬细胞集落刺激因子和/或类固醇对支气管肺泡巨噬细胞响应烟曲霉菌分生孢子产生促炎细胞因子和趋化因子的调节作用。

Regulation by granulocyte-macrophage colony-stimulating factor and/or steroids given in vivo of proinflammatory cytokine and chemokine production by bronchoalveolar macrophages in response to Aspergillus conidia.

作者信息

Brummer Elmer, Kamberi Marika, Stevens David A

机构信息

Department of Medicine, Division of Infectious Diseases, Santa Clara Valley Medical Center, and California Institute for Medical Research, San Jose, California 95128-2669, USA.

出版信息

J Infect Dis. 2003 Feb 15;187(4):705-9. doi: 10.1086/368383. Epub 2003 Feb 7.

DOI:10.1086/368383
PMID:12599092
Abstract

Production of the proinflammatory cytokines interleukin (IL)-1 alpha and tumor necrosis factor (TNF)-alpha and of the chemotactic chemokine macrophage inflammatory protein (MIP)-1 alpha by bronchoalveolar macrophages (BAMs) from mice in response to Aspergillus conidia was tested after in vivo administration of saline, dexamethasone, cortisone acetate, granulocyte-macrophage colony-stimulating factor (GM-CSF), or a combination. Dexamethasone suppressed production of IL-1 alpha, TNF-alpha, and MIP-1 alpha; GM-CSF reduced secretion slightly but antagonized dexamethasone suppression when the two were given in combination. Cortisone acetate gave results similar to dexamethasone, but cortisone acetate suppression of BAM responses lasted 7 days, > or = 4 days longer than dexamethasone suppression. The effect of GM-CSF on cortisone acetate suppression lasted at least 7 days. GM-CSF could promote resistance to conidia by maintaining proinflammatory responses.

摘要

在对小鼠进行体内给予生理盐水、地塞米松、醋酸可的松、粒细胞-巨噬细胞集落刺激因子(GM-CSF)或联合用药后,检测了支气管肺泡巨噬细胞(BAM)对烟曲霉菌分生孢子产生促炎细胞因子白细胞介素(IL)-1α和肿瘤坏死因子(TNF)-α以及趋化性趋化因子巨噬细胞炎性蛋白(MIP)-1α的情况。地塞米松抑制IL-1α、TNF-α和MIP-1α的产生;GM-CSF略微降低分泌,但当二者联合给予时可拮抗地塞米松的抑制作用。醋酸可的松的结果与地塞米松相似,但醋酸可的松对BAM反应的抑制持续7天,比地塞米松抑制长≥4天。GM-CSF对醋酸可的松抑制的作用至少持续7天。GM-CSF可通过维持促炎反应来促进对分生孢子的抵抗力。

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