Interleukin-1 and host control of pulmonary histoplasmosis
Interleukin-1 and host control of pulmonary histoplasmosis
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DOI：
10.1086/506946
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发表时间：
2006-09-15
影响因子：
6.4
通讯作者：
McGuinness, Michael
中科院分区：
文献类型：
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作者：
Deepe, George S., Jr.;McGuinness, Michael
我们发现，白细胞介素（IL）-1b水平升高的小鼠感染组织胞浆菌的肺。因此，我们研究了IL-1 β和IL-1信号对宿主防御肺组织胞浆菌病的影响。在IL-1受体1敲除（IL-1 R（-/-））小鼠的挑战，真菌感染后第7天的恢复超过野生型（WT）小鼠。IL-1 β的抗体中和也加重了感染。对于两组小鼠，缺乏生物活性细胞因子导致高比例小鼠无法控制感染。信号传导的缺乏对继发性组织胞浆菌病小鼠的宿主抗性有适度的影响。在IL-1 R（-/-）小鼠的肺中检测到宿主防御机制的几种扰动。CD 4（+）细胞数量减少，诱导型一氧化氮合酶基因的转录被短暂抑制。与WT小鼠肺中的IL-4和IL-10水平相比，IL-1 R（-/-）小鼠肺中的IL-4和IL-10水平升高。相反，干扰素-γ水平降低。因此，IL-1有助于宿主抵抗H.胶囊。
We found that interleukin (IL)-1b levels were elevated in the lungs of mice infected with Histoplasma capsulatum. Hence, we examined the influence that IL-1 beta and IL-1 signaling has on host defenses against pulmonary histoplasmosis. In IL-1 receptor 1 knockout (IL-1R(-/-)) mice challenged intratracheally, fungal recovery on day 7 after infection exceeded that in wild-type (WT) mice. Antibody neutralization of IL-1 beta also exacerbated infection. For both groups of mice, the absence of bioactive cytokine led to a failure to control infection in a high proportion of mice. The absence of signaling had a modest effect on host resistance in mice with secondary histoplasmosis. Several perturbations in host defense mechanisms were detected in the lungs of IL-1R(-/-) mice. The number of CD4(+) cells was decreased, and transcription of the gene for inducible nitric oxide synthase was depressed transiently. IL-4 and IL-10 levels were elevated in the lungs of IL-1R(-/-) mice, compared with those in the lungs of WT mice. Conversely, interferon-gamma levels were decreased. Thus, IL-1 contributes to host resistance to infection with H. capsulatum.