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原代大鼠II型肺泡细胞产生细胞因子诱导的中性粒细胞趋化因子

Cytokine-induced neutrophil chemoattractant production by primary rat alveolar type II cells.

作者信息

Crippen T L, Klasing K C, Hyde D M

机构信息

Department of Anatomy, Physiology and Cell Biology, University of California, Davis 95616, USA.

出版信息

Inflammation. 1995 Oct;19(5):575-86. doi: 10.1007/BF01539137.

Abstract

This study was designed to determine the production of the chemokine cytokine-induced neutrophil chemoattractant (CINC) by primary rat alveolar type II (ATII) cells upon stimulation with exogenous and endogenous proinflammatory factors. Cultures of primary rat ATII cells were exposed to lipopolysaccharide (LPS), interleukin-1 beta (IL-1 beta) or tumor necrosis factor-alpha (TNF alpha) over a 16 hour period and the production of CINC both apically and basolaterally was measured by ELISA. Compared to unstimulated (UNS) cultures, LPS, IL-1 beta and TNF alpha were found to significantly increase the level of CINC detected in culture by two, four and sixteen hours post stimulation, respectively. ATII cells also demonstrated a polar secretion of CINC. The accumulation of CINC basolaterally was significantly more than apically; 133%, 45%, 117% and 123% for UNS, IL-1 beta, LPS and TNF alpha respectively. We demonstrated that primary rat ATII cells may participate in the chemokine network during inflammation by the production of CINC upon stimulation with endogenous and exogenous factors.

摘要

本研究旨在确定原代大鼠Ⅱ型肺泡上皮(ATII)细胞在外源性和内源性促炎因子刺激下趋化因子细胞因子诱导的中性粒细胞趋化因子(CINC)的产生情况。将原代大鼠ATII细胞培养物在16小时内暴露于脂多糖(LPS)、白细胞介素-1β(IL-1β)或肿瘤坏死因子-α(TNFα),并通过酶联免疫吸附测定(ELISA)测量顶侧和基底外侧CINC的产生情况。与未刺激(UNS)的培养物相比,发现LPS、IL-1β和TNFα分别在刺激后2小时、4小时和16小时显著增加了培养物中检测到的CINC水平。ATII细胞还表现出CINC的极性分泌。基底外侧CINC的积累明显多于顶侧;未刺激组、IL-1β组、LPS组和TNFα组分别为133%、45%、117%和123%。我们证明,原代大鼠ATII细胞在受到内源性和外源性因子刺激时,可能通过产生CINC参与炎症过程中的趋化因子网络。

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