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细菌性肺炎和结节病过程中肺泡巨噬细胞自发释放粒细胞集落刺激因子(G-CSF):支气管肺泡灌洗回收细胞中内毒素依赖性和非内毒素依赖性G-CSF释放

Spontaneous release of granulocyte colony-stimulating factor (G-CSF) by alveolar macrophages in the course of bacterial pneumonia and sarcoidosis: endotoxin-dependent and endotoxin-independent G-CSF release by cells recovered by bronchoalveolar lavage.

作者信息

Tazi A, Nioche S, Chastre J, Smiéjan J M, Hance A J

机构信息

INSERM U.82, Faculté de Médecine Xavier Bichat, Paris, France.

出版信息

Am J Respir Cell Mol Biol. 1991 Feb;4(2):140-7. doi: 10.1165/ajrcmb/4.2.140.

DOI:10.1165/ajrcmb/4.2.140
PMID:1703767
Abstract

Because granulocyte colony-stimulating factor (G-CSF) is known to induce granulopoiesis and activate mature neutrophils, this factor could be important in determining the number and functional activity of neutrophils at sites of lung disease. The purpose of this study was to evaluate the ability of lung immune and inflammatory cells to produce G-CSF, and to seek evidence for the spontaneous production of this factor by cells recovered by lavage from controls and patients with lung diseases in which neutrophils may play a pathogenetic role. Lavage cells from controls produced little G-CSF spontaneously. Alveolar macrophages (AM), but not lymphocytes, produced large amounts following endotoxin stimulation. Lavage cells from patients with respiratory failure associated with bacterial pneumonia, but not those with respiratory failure from noninfectious causes, spontaneously released G-CSF (32 +/- 24 and less than 1 U/10(6) AM, respectively). Lavage cells from five of 15 patients with sarcoidosis and one of five patients with diffuse pulmonary fibrosis also spontaneously released G-CSF, which could not be explained by endotoxin exposure. The release of G-CSF by endotoxin-dependent and -independent mechanisms could play a role in the recruitment and activation of neutrophils in bacterial pneumonia and participate in the pathogenesis of some interstitial lung diseases.

摘要

由于已知粒细胞集落刺激因子(G-CSF)可诱导粒细胞生成并激活成熟中性粒细胞,因此该因子在决定肺部疾病部位中性粒细胞的数量和功能活性方面可能很重要。本研究的目的是评估肺免疫细胞和炎症细胞产生G-CSF的能力,并寻找从对照者以及中性粒细胞可能起致病作用的肺部疾病患者中通过灌洗回收的细胞自发产生该因子的证据。对照者的灌洗细胞自发产生的G-CSF很少。内毒素刺激后,肺泡巨噬细胞(AM)而非淋巴细胞产生大量G-CSF。与细菌性肺炎相关的呼吸衰竭患者的灌洗细胞可自发释放G-CSF(分别为32±24和小于1 U/10⁶ AM),而非感染性原因导致呼吸衰竭的患者则不能。15例结节病患者中的5例以及5例弥漫性肺纤维化患者中的1例的灌洗细胞也自发释放G-CSF,这无法用内毒素暴露来解释。内毒素依赖性和非依赖性机制导致的G-CSF释放可能在细菌性肺炎中中性粒细胞的募集和激活中起作用,并参与某些间质性肺病的发病机制。

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