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伯克霍尔德菌中存在过度的炎症反应,该反应由囊性纤维化患者来源的人巨噬细胞介导。

Exaggerated inflammatory responses mediated by Burkholderia cenocepacia in human macrophages derived from Cystic fibrosis patients.

机构信息

Section of Pediatric Pulmonology, Nationwide Children's Hospital, Columbus, OH, United States.

出版信息

Biochem Biophys Res Commun. 2012 Jul 27;424(2):221-7. doi: 10.1016/j.bbrc.2012.06.066. Epub 2012 Jun 20.

DOI:10.1016/j.bbrc.2012.06.066
PMID:22728038
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3408781/
Abstract

Cystic fibrosis (CF) is accompanied with heightened inflammation worsened by drug resistant Burkholderia cenocepacia. Human CF macrophage responses to B. cenocepacia are poorly characterized and variable in the literature. Therefore, we examined human macrophage responses to the epidemic B. cenocepacia J2315 strain in order to identify novel anti-inflammatory targets. Peripheral blood monocyte derived macrophages were obtained from 23 CF and 27 non-CF donors. Macrophages were infected with B. cenocepacia J2315 and analyzed for cytokines, cytotoxicity, and microscopy. CF macrophages demonstrated significant increases in IL-1β, IL-10, MCP-1, and IFN-γ production in comparison to non-CF controls. CF patients on prednisone exhibited globally diminished cytokines compared to controls and other CF patients. CF macrophages also displayed increased bacterial burden and cell death. In conclusion, CF macrophages demonstrate exaggerated IL-1β, IL-10, MCP-1, and IFN-γ production and cell death during B. cenocepacia infection. Treatment with corticosteroids acutely suppressed cytokine responses.

摘要

囊性纤维化(CF)伴有炎症加剧,而耐药物的洋葱伯克霍尔德菌(Burkholderia cenocepacia)会使炎症恶化。人类 CF 巨噬细胞对 B. cenocepacia 的反应在文献中描述甚少且存在差异。因此,我们研究了人类巨噬细胞对流行的 B. cenocepacia J2315 菌株的反应,以确定新的抗炎靶点。从 23 名 CF 和 27 名非 CF 供体中获得外周血单核细胞衍生的巨噬细胞。用 B. cenocepacia J2315 感染巨噬细胞,并分析细胞因子、细胞毒性和显微镜检查。与非 CF 对照组相比,CF 巨噬细胞产生的 IL-1β、IL-10、MCP-1 和 IFN-γ 显著增加。接受强的松治疗的 CF 患者与对照组和其他 CF 患者相比,细胞因子总体减少。CF 巨噬细胞还显示出增加的细菌负荷和细胞死亡。总之,CF 巨噬细胞在 B. cenocepacia 感染期间表现出过度的 IL-1β、IL-10、MCP-1 和 IFN-γ 产生和细胞死亡。皮质类固醇治疗急性抑制细胞因子反应。

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