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首页> 外文期刊>Infection and immunity >The CXC Chemokines Gamma Interferon (IFN-γ)-Inducible Protein 10 and Monokine Induced by IFN-γ Are Released during Severe Melioidosis
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The CXC Chemokines Gamma Interferon (IFN-γ)-Inducible Protein 10 and Monokine Induced by IFN-γ Are Released during Severe Melioidosis

机译:CXC趋化因子γ干扰素(IFN-γ)诱导蛋白10和IFN-γ诱导的单核因子在严重的类胡萝卜素病期间释放

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Gamma interferon (IFN-γ)-inducible protein 10 (IP-10) and monokine induced by IFN-γ (Mig) are related CXC chemokines which bind to the CXCR3 receptor and specifically target activated T lymphocytes and natural killer (NK) cells. The production of IP-10 and Mig by various cell types in vitro is strongly dependent on IFN-γ. To determine whether IP-10 and Mig are released during bacterial infection in humans, we measured plasma levels of IP-10 and Mig in patients with melioidosis, a severe gram-negative infection caused byBurkholderia pseudomallei. IP-10 and Mig were markedly elevated in patients with melioidosis on admission, particularly in blood culture-positive patients, and remained elevated during the 72-h study period. Levels of IP-10 and Mig showed a positive correlation with IFN-γ concentrations and also correlated with clinical outcome. In whole blood stimulated with heat-killed B. pseudomallei, neutralization of IFN-γ and tumor necrosis factor alpha (TNF-α) partly attenuated IP-10 and Mig release, while anti-interleukin-12 (IL-12) and anti-IL-18 had a synergistic effect. Stimulation with other bacteria or endotoxin also induced strong secretion of IP-10 and Mig. These data suggest that IP-10 and Mig are part of the innate immune response to bacterial infection. IP-10 and Mig may contribute to host defense in Th1-mediated host defense during infections by attracting CXCR3+ Th1 cells to the site of inflammation.
机译:γ-干扰素(IFN-γ)诱导蛋白10(IP-10)和由IFN-γ(Mig)诱导的单因子是相关的CXC趋化因子,它们与CXCR3受体结合,并特别靶向活化的T淋巴细胞和自然杀伤(NK)细胞。各种细胞类型在体外产生IP-10和Mig的过程强烈依赖于IFN-γ。为了确定在人类细菌感染过程中IP-10和Mig是否释放,我们测量了类拟鼻osis病患者的血浆IP-10和Mig的水平,类拟南芥是由假阳性伯克霍尔德氏菌引起的严重革兰氏阴性感染。 IP-10和Mig在入院的类胡osis病患者中明显升高,尤其是在血培养阳性患者中,并在72小时的研究期间保持升高。 IP-10和Mig的水平与IFN-γ浓度呈正相关,也与临床结果相关。用热杀死的 B刺激的全血。假性疟原虫,IFN-γ和肿瘤坏死因子α(TNF-α)的中和部分减弱了IP-10和Mig的释放,而抗白介素12(IL-12)和抗IL-18具有协同作用影响。用其他细菌或内毒素刺激也会诱导IP-10和Mig的强烈分泌。这些数据表明IP-10和Mig是对细菌感染的固有免疫反应的一部分。 IP-10和Mig通过将CXCR3 + Th1细胞吸引到炎症部位,可能在感染过程中有助于Th1介导的宿主防御。

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