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.
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。
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