Cytokine- and T helper-dependent lung mucosal immunity in mice with invasive pulmonary aspergillosis
Cytokine- and T helper-dependent lung mucosal immunity in mice with invasive pulmonary aspergillosis
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DOI：
10.1086/314493
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发表时间：
1998-12-01
影响因子：
6.4
通讯作者：
Romani, L
中科院分区：
文献类型：
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作者：
Cenci, E;Mencacci, A;Romani, L
研究了细胞因子和辅助性T细胞（Th）依赖的肺黏膜抗真菌免疫在小鼠侵袭性肺曲霉病（IPA）中的作用。完整的或白细胞减少的DBA/2小鼠分别对多次鼻内注射活的烟曲霉分生孢子引起的感染具有抗性或高度易感性。抗性与肺吞噬细胞的未受损的先天抗真菌活性相关，同时，肿瘤坏死因子（TNF）-α和白细胞介素（IL）-12的高水平产生以及产生干扰素-γ和IL-12的间质淋巴细胞的存在，2.相反，TNF-α和IL-12的产生在高度易感小鼠中下调，这些小鼠也具有先天性抗真菌免疫缺陷和肺淋巴细胞高水平的IL-4和IL-10产生。在局部IL-4或IL-10中和或IL-12给药后，易感小鼠的耐药性增加。这些结果表明，类似于在小鼠播散性曲霉菌病，先天性和Th 1依赖性免疫在宿主防御IPA发挥重要作用。
The role of cytokine- and T helper (Th)-dependent lung mucosal antifungal immunity in murine invasive pulmonary aspergillosis (IPA) was investigated. Intact or leukopenic DBA/2 mice were resistant or highly susceptible, respectively, to infection caused by multiple intranasal injections of viable Aspergillus fumigatus conidia, Resistance was associated with unimpaired innate antifungal activity of pulmonary phagocytic cells, concomitant, with high-level production of tumor necrosis factor (TNF)-alpha and interleukin (IL)-12 and the presence of interstitial lymphocytes producing interferon-gamma and IL-2. Conversely, production of TNF-alpha and IL-12 was down-regulated in highly susceptible mice, which also had defective innate antifungal immunity and high-level production of IL-4 and IL-10 by lung lymphocytes. Resistance was increased in susceptible mice upon local IL-4 or IL-10 neutralization or IL-12 administration. These results indicate that, similar to observations in mice with disseminated aspergillosis, innate and Th1-dependent immunity play an essential role in host defense against IPA.