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Cytokines, sepsis and immunomodulation.细胞因子、脓毒症与免疫调节
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2
Acute pulmonary coccidioidomycosis mimicking bacterial pneumonia and septic shock: a report of two cases.酷似细菌性肺炎和感染性休克的急性肺球孢子菌病:两例报告
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In vitro production of tumor necrosis factor-alpha by adherent human peripheral blood mononuclear cells incubated with killed coccidioidal arthroconidia and spherules.用灭活的球孢子菌关节分生孢子和球形体培养贴壁人外周血单个核细胞体外产生肿瘤坏死因子-α
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Cytokine induction in human coccidioidomycosis.人类球孢子菌病中的细胞因子诱导
Infect Immun. 1994 Sep;62(9):3980-3. doi: 10.1128/iai.62.9.3980-3983.1994.
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Detection of in vivo expression of interleukin-10 using a semi-quantitative polymerase chain reaction method in Schistosoma mansoni infected mice.采用半定量聚合酶链反应法检测曼氏血吸虫感染小鼠体内白细胞介素-10的表达
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Coccidioidomycosis: factors affecting the host-parasite interaction.球孢子菌病:影响宿主-寄生虫相互作用的因素
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Genetic control of resistance to Coccidioides immitis: a single gene that is expressed in spleen cells determines resistance.对粗球孢子菌抗性的遗传控制:一个在脾细胞中表达的单基因决定抗性。
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Induction and expression of cell-mediated immune responses in inbred mice infected with Coccidioides immitis.感染粗球孢子菌的近交系小鼠中细胞介导免疫反应的诱导与表达
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Fungicidal activation of murine macrophages by recombinant gamma interferon.重组γ干扰素对小鼠巨噬细胞的杀菌激活作用
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小鼠球孢子菌病期间肿瘤坏死因子α、白细胞介素-1α和白细胞介素-6的产生

Production of tumor necrosis factor alpha, interleukin-1 alpha, and interleukin-6 during murine coccidioidomycosis.

作者信息

Cox R A, Magee D M

机构信息

Department of Research Immunology, Texas Center for Infectious Disease, San Antonio 78223-3597, USA.

出版信息

Infect Immun. 1995 Oct;63(10):4178-80. doi: 10.1128/iai.63.10.4178-4180.1995.

DOI:10.1128/iai.63.10.4178-4180.1995
PMID:7558338
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC173589/
Abstract

The proinflammatory cytokines tumor necrosis factor alpha (TNF-alpha), interleukin-1 alpha (IL-1 alpha), and interleukin-6 (IL-6) were induced in mice infected with Coccidioides immitis. Analyses of the cytokine profiles of two inbred mouse strains which differ in their susceptibility to pulmonary challenge with C. immitis revealed higher levels of IL-6 in lungs from DBA/2 mice (resistant strain) than in those from BALB/c mice (susceptible strain) beginning at day 6 and continuing through day 15 postinfection. Spleen cells from both mouse strains secreted TNF-alpha, IL-1 alpha, and IL-6 in vitro in response to stimulation with killed spherules but differed in that spleen cells from the resistant strain produced increased levels of these cytokines earlier after pulmonary challenge and at increased levels throughout the course of the disease.

摘要

在感染粗球孢子菌的小鼠中诱导产生了促炎细胞因子肿瘤坏死因子α(TNF-α)、白细胞介素-1α(IL-1α)和白细胞介素-6(IL-6)。对两种近交系小鼠品系的细胞因子谱进行分析,这两种品系对粗球孢子菌肺部攻击的易感性不同,结果显示,从感染后第6天开始直至第15天,DBA/2小鼠(抗性品系)肺中的IL-6水平高于BALB/c小鼠(易感品系)肺中的IL-6水平。两种小鼠品系的脾细胞在体外受到灭活小球刺激后均分泌TNF-α、IL-1α和IL-6,但不同的是,抗性品系的脾细胞在肺部攻击后更早产生这些细胞因子,且在疾病全过程中其水平均有所升高。