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解脲脲原体诱导巨噬细胞产生促炎细胞因子。

Ureaplasma urealyticum-induced production of proinflammatory cytokines by macrophages.

作者信息

Li Y H, Brauner A, Jonsson B, van der Ploeg I, Söder O, Holst M, Jensen J S, Lagercrantz H, Tullus K

机构信息

Astrid Lindgren Children's Hospital, Karolinska Hospital, Stockholm, Sweden.

出版信息

Pediatr Res. 2000 Jul;48(1):114-9. doi: 10.1203/00006450-200007000-00020.

DOI:10.1203/00006450-200007000-00020
PMID:10879809
Abstract

Ureaplasma urealyticum is relatively common in the respiratory tract of very low birth weight infants and has been hypothesized to be involved in the development of chronic lung disease. The purpose of this study was to investigate whether U. urealyticum could stimulate macrophages to produce proinflammatory cytokines in vitro, which are early pathologic changes in the lung during the development of chronic lung disease. A human monocytic cell line (THP-1) differentiated to macrophages, a rat alveolar macrophage cell line (Nr8383), and human lung macrophages from tracheobronchial aspirate fluid in preterm infants were exposed to U. urealyticum antigen for 24 h. The protein levels of human IL-6, tumor necrosis factor-alpha (TNF-alpha), and rat TNF-alpha were measured with ELISA. Rat IL-6 was analyzed with a specific bioassay. The mRNA levels of these cytokines were detected by reverse transcriptase-PCR. The production of TNF-alpha and IL-6 increased after stimulation with U. urealyticum in both the human and rat macrophage cell lines. In tracheobronchial aspirate fluid macrophages, U. urealyticum increased the production of TNF-alpha from 14 to 84% and IL-6 from 46 to 268% above control levels. U. urealyticum also induced gene expression of TNF-alpha and IL-6. In conclusion, U. urealyticum could be an important factor in the development of chronic lung disease because of its ability to induce alveolar macrophage proinflammatory cytokine production.

摘要

解脲脲原体在极低出生体重儿的呼吸道中相对常见,据推测其与慢性肺病的发生有关。本研究的目的是调查解脲脲原体在体外是否能刺激巨噬细胞产生促炎细胞因子,而促炎细胞因子是慢性肺病发展过程中肺部早期的病理变化。将分化为巨噬细胞的人单核细胞系(THP-1)、大鼠肺泡巨噬细胞系(Nr8383)以及来自早产儿气管支气管吸出液的人肺巨噬细胞暴露于解脲脲原体抗原24小时。用酶联免疫吸附测定法测量人白细胞介素-6(IL-6)、肿瘤坏死因子-α(TNF-α)以及大鼠TNF-α的蛋白水平。用特定的生物测定法分析大鼠IL-6。通过逆转录聚合酶链反应检测这些细胞因子的mRNA水平。在人和大鼠巨噬细胞系中,用解脲脲原体刺激后,TNF-α和IL-6的产生均增加。在气管支气管吸出液巨噬细胞中,解脲脲原体使TNF-α的产生比对照水平增加了14%至84%,使IL-6的产生比对照水平增加了46%至268%。解脲脲原体还诱导了TNF-α和IL-6的基因表达。总之,解脲脲原体因其诱导肺泡巨噬细胞产生促炎细胞因子的能力,可能是慢性肺病发生发展中的一个重要因素。

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