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首页> 外文期刊>Infection and immunity >Absence of Interleukin-4 Determines Less Severe Pulmonary Paracoccidioidomycosis Associated with Impaired Th2 Response
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Absence of Interleukin-4 Determines Less Severe Pulmonary Paracoccidioidomycosis Associated with Impaired Th2 Response

机译：白细胞介素4的缺乏确定与Th2反应受损相关的严重程度较轻的肺副球菌病

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Host resistance to paracoccidiodomycosis, the main deep mycosis in Latin America, is mainly due to cellular immunity and gamma interferon (IFN-γ) production. To assess the role of interleukin-4 (IL-4), a Th2-inducing cytokine, pulmonary paracoccidioidomycosis was studied in IL-4-deficient (IL-4?/?) and wild-type (WT) C57BL/6 mice at the innate and acquired phases of immune response. Forty-eight hours after infection, equivalent numbers of viable Paracoccidioides brasiliensis yeast cells were recovered from the lungs of IL-4?/? and WT mice intratracheally infected with one million fungal cells. Alveolar macrophages from infected IL-4?/? mice controlled in vitro fungal growth more efficiently than macrophages from WT mice and secreted higher levels of nitric oxide. Compared with WT mice, IL-4?/? animals presented increased levels of pulmonary IFN-γ and augmented polymorphonuclear leukocyte influx to the lungs. Decreased pulmonary fungal loads were characterized in deficient mice at week 2 postinfection, concomitant with diminished presence of IL-10. At week 8, lower numbers of yeasts were recovered from lungs and liver of IL-4?/? mice associated with increased production of IFN-γ but impaired synthesis of IL-5 and IL-10. However, a clear shift to a Th1 pattern was not characterized, since IL-4?/? mice did not alter delayed-type hypersensitivity anergy or IL-2 levels. In addition, IL-4 deficiency resulted in significantly reduced levels of pulmonary IL-12, granulocyte-macrophage colony-stimulating factor, IL-3, monocyte chemotactic protein 1, and specific antibody isotypes. In IL-4?/? mice, well-organized granulomas restraining fungal cells replaced the more extensive lesions containing high numbers of fungi and inflammatory leukocytes developed by IL-4-sufficient mice. These results clearly showed that genetically determined deficiency of IL-4 can exert a protective role in pulmonary paracoccidioidomycosis.
机译：寄主对副球菌病的宿主抗性是拉丁美洲的主要深部真菌病，主要归因于细胞免疫力和γ-干扰素（IFN-γ）的产生。为了评估IL-4缺陷型（IL-4 ？/？）和野生型（IL-4）（一种Th2诱导的细胞因子，肺旁球虫病）的白介素-4（IL-4）的作用。 WT）C57BL / 6小鼠处于免疫反应的先天和后天阶段。感染后48小时，从IL-4 ？/？的肺和气管内感染了100万真菌的WT小鼠的肺中回收了同等数量的巴西乳杆菌（Paracoccidioides brasiliensis）活酵母细胞。细胞。被感染的IL-4 α/β小鼠的肺泡巨噬细胞比野生型小鼠的巨噬细胞更有效地控制了体外真菌的生长，并分泌了更高水平的一氧化氮。与野生型小鼠相比，IL-4 ？/？动物的肺IFN-γ水平升高，多形核白细胞向肺的流入增加。感染后第2周，缺陷小鼠的肺真菌负荷降低，并伴有IL-10的减少。在第8周时，IL-4 α/β小鼠的肺和肝脏中酵母菌的数量减少，这与IFN-γ的产生增加有关，但IL-5和IL-10的合成受损。然而，由于IL-4 α/β小鼠没有改变迟发型超敏反应的无反应性或IL-2的水平，因此没有明确的转变为Th1模式。另外，IL-4缺乏导致肺IL-12，粒细胞-巨噬细胞集落刺激因子，IL-3，单核细胞趋化蛋白1和特定抗体同种型水平显着降低。在IL-4 ？/？小鼠中，组织良好的肉芽肿抑制真菌细胞取代了由IL-4充足的小鼠所形成的更广泛的病灶，其中含有大量真菌和炎性白细胞。这些结果清楚地表明，遗传学上确定的IL-4缺乏可以在肺副球虫病中发挥保护作用。

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