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β趋化因子在患有支原体呼吸道疾病的小鼠肺部产生。

Beta-chemokines are produced in lungs of mice with mycoplasma respiratory disease.

作者信息

Simecka J W

机构信息

Department of Molecular Biology and Immunology, 3500 Camp Bowie Blvd. University of North Texas Health Science Center, Fort Worth, TX 76107, USA.

出版信息

Curr Microbiol. 1999 Sep;39(3):163-7. doi: 10.1007/s002849900439.

Abstract

The recruitment of mononuclear cells in lungs is a key event in the pathogenesis of mycoplasma respiratory disease, but the cascade of events responsible is unknown. Studies were conducted to determine whether beta-chemokines, which are chemotactic for lymphocytes and macrophages, are produced in murine mycoplasma respiratory disease. Our results show that mRNA expression of the macrophage chemoattractant factor (MCP-1) and macrophage inflammatory peptides (MIP-1alpha and MIP-1beta), but not RANTES, increases in Mycoplasma pulmonis-infected mice. Also, MCP-1 concentrations were much higher in lung extracts from mycoplasma-infected mice than in uninfected mice. As beta-chemokines are chemotactic for lymphocytes and macrophages, these results suggest that MCP-1, MIP-1alpha, and/or MIP-1beta, but not RANTES, contribute to mononuclear cell infiltration associated with murine mycoplasma respiratory disease. Thus, the activation of cells to produce beta-chemokines is associated with mycoplasma infection, and the beta-chemokines, along with other factors and cytokines, are most likely involved in the cascade of events leading to mycoplasma inflammatory disease.

摘要

肺部单核细胞的募集是支原体呼吸道疾病发病机制中的关键事件,但引发这一系列事件的过程尚不清楚。我们开展了多项研究,以确定对淋巴细胞和巨噬细胞具有趋化作用的β趋化因子是否在小鼠支原体呼吸道疾病中产生。我们的结果表明,在感染肺支原体的小鼠中,巨噬细胞趋化因子(MCP-1)和巨噬细胞炎症肽(MIP-1α和MIP-1β)的mRNA表达增加,但调节激活正常T细胞表达和分泌的因子(RANTES)的mRNA表达未增加。此外,支原体感染小鼠的肺提取物中MCP-1浓度比未感染小鼠的高得多。由于β趋化因子对淋巴细胞和巨噬细胞具有趋化作用,这些结果表明,MCP-1、MIP-1α和/或MIP-1β而非RANTES,促成了与小鼠支原体呼吸道疾病相关的单核细胞浸润。因此,细胞被激活以产生β趋化因子与支原体感染有关,并且β趋化因子与其他因子和细胞因子一起,很可能参与了导致支原体炎症性疾病的一系列事件。

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