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首页> 外文期刊>Infection and immunity >Ascaris suum-Derived Products Suppress Mucosal Allergic Inflammation in an Interleukin-10-Independent Manner via Interference with Dendritic Cell Function
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Ascaris suum-Derived Products Suppress Mucosal Allergic Inflammation in an Interleukin-10-Independent Manner via Interference with Dendritic Cell Function

机译：scar虫来源的产品通过干扰树突状细胞功能以白介素10独立的方式抑制粘膜过敏性炎症。

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We have previously demonstrated that protection from allergic inflammation by Ascaris suum infection was characterized by a global increase in interleukin-10 (IL-10) and the development of protective CD4+/CD25+ T cells (L. Schopf, S. Luccioli, V. Bundoc, P. Justice, C. C. Chan, B. J. Wetzel, H. H. Norris, J. F. Urban, Jr., and A. Keane-Myers, Investig. Ophthalmol. Vis. Sci. >46:2772-2780, 2005). Here, we used A. suum pseudocoelomic fluid (PCF) in lieu of infection to define molecular mechanisms of allergic protection in a mouse model of allergic inflammation. Mice were sensitized with ragweed (RW) and PCF (RW/PCF), PCF alone, or RW alone and then challenged intratracheally, intranasally, and supraocularly with RW. Histological examination of the eyes and lungs, analysis of the bronchoalveolar lavage fluid (BALF), and characterization of ex vivo cytokine responses were performed to determine allergic inflammatory responses. RW/PCF-treated mice had suppressed allergic immune responses compared to mice given RW alone. To investigate whether IL-10 was involved in PCF-mediated allergic protection, similar experiments were performed using mice genetically deficient for IL-10. Persistent protection from allergic disease was observed in the absence of IL-10, indicating the primary mechanism of PCF protection is IL-10 independent. Ex vivo and in vitro analysis of PCF-treated dendritic cells (DC) demonstrated reduced activation receptor expression and cytokine production in response to either RW or lipopolysaccharide stimulation. These findings extend previous studies that showed infection with A. suum alters expression of allergic disease and suggest that PCF can contribute to this effect by interference with DC function.
机译：先前我们已经证明， A虫病感染对过敏性炎症的保护作用以白介素10（IL-10）的整体增加和保护性CD4 + /的发展为特征。 CD25 + T细胞（L. Schopf，S。Luccioli，V。Bundoc，P.Justice，CC Chan，BJ Wetzel，HH Norris，JF Urban，Jr。和A. Keane-Myers，眼科与视觉科学调查》，> 46： 2772-2780，2005年）。在这里，我们使用 A。 suum 假结肠腔积液（PCF）代替感染，以定义过敏性炎症小鼠模型中的过敏性保护分子机制。用豚草（RW）和PCF（RW / PCF），单独的PCF或单独的RW致敏小鼠，然后用RW气管内，鼻内和眼上攻击。进行了眼睛和肺的组织学检查，支气管肺泡灌洗液（BALF）的分析以及离体细胞因子反应的表征，以确定过敏性炎症反应。与仅给予RW的小鼠相比，用RW / PCF处理的小鼠抑制了过敏性免疫反应。为了研究IL-10是否参与PCF介导的过敏性保护，使用遗传上缺乏IL-10的小鼠进行了类似的实验。在没有IL-10的情况下观察到了对过敏性疾病的持久保护，这表明PCF保护的主要机制是IL-10独立的。对PCF处理的树突状细胞（DC）进行离体和体外分析表明，响应RW或脂多糖刺激，激活受体的表达减少和细胞因子产生减少。这些发现扩展了以前的研究，这些研究表明感染了 A。 suum 会改变过敏性疾病的表达，并提示PCF可以通过干扰DC功能来促进这种作用。

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