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首页> 外文期刊>Infection and immunity >Anisakis pegreffii-Induced Airway Hyperresponsiveness Is Mediated by Gamma Interferon in the Absence of Interleukin-4 Receptor Alpha Responsiveness
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Anisakis pegreffii-Induced Airway Hyperresponsiveness Is Mediated by Gamma Interferon in the Absence of Interleukin-4 Receptor Alpha Responsiveness

机译：在白介素4受体α缺乏的情况下，γ-干扰素介导了由茴香提取物诱导的气道高反应性。

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Infection with the fish parasite Anisakis following exposure to contaminated fish can lead to allergic reactions in humans. The present study examined the immunological mechanisms underlying the development of allergic airway inflammation in mice after different routes of sensitization to Anisakis. Wild-type and interleukin-4 receptor alpha (IL-4Rα)-deficient BALB/c mice were sensitized intraperitoneally with live or heat-killed Anisakis larvae or by intranasal administration of an Anisakis extract and were subsequently challenged intranasally with an Anisakis extract. Both routes of sensitization induced IL-4Rα-dependent allergic airway responses, whereas allergen-specific antibody responses developed only when mice were sensitized intraperitoneally. Intranasal sensitization induced airway hyperresponsiveness (AHR) in wild-type mice only, showing that AHR was IL-4/IL-13 dependent. Unexpectedly, infection with Anisakis larvae induced AHR in both wild-type and IL-4Rα-deficient mice. IL-4Rα-independent AHR was mediated by gamma interferon (IFN-γ), as evidenced by the fact that in vivo neutralization of IFN-γ abrogated AHR. Together, these results demonstrate that both infection with larvae and inhalational exposure to Anisakis proteins are potent routes of allergic sensitization to Anisakis, explaining food- and work-related allergies in humans. Importantly for diagnosis, allergic airway inflammation can be independent of detectable Anisakis-specific antibodies. Moreover, depending on the route of sensitization, AHR can be induced either by IL-4/IL-13 or by IFN-γ.
机译：暴露于受污染的鱼后感染鱼寄生虫可能导致人类过敏反应。本研究探讨了不同的对 Anisakis 致敏途径后小鼠过敏性气道炎症发展的免疫机制。将野生型和白介素4受体α（IL-4Rα）缺陷的BALB / c小鼠腹膜内用活的或加热杀死的 Anisakis 幼虫或鼻内施用 Anisakis 致敏em>提取物，随后用 Anisakis 提取物鼻内攻击。两种致敏途径均诱导依赖IL-4Rα的过敏性气道反应，而仅当小鼠腹膜内致敏时，才会产生过敏原特异性抗体反应。鼻内敏化仅在野生型小鼠中诱导气道高反应性（AHR），表明AHR是IL-4 / IL-13依赖性的。出乎意料的是，在野生型和IL-4Rα缺陷型小鼠中，感染 Anisakis 幼虫都会诱发AHR。 IL-4Rα独立的AHR是由γ-干扰素（IFN-γ）介导的，这由IFN-γ的体内中和作用消除了AHR的事实证明。在一起，这些结果表明，幼虫感染和吸入 Anisakis 蛋白都是对 Anisakis 致敏的有效途径，解释了人类与食物和工作有关的过敏。对于诊断很重要，过敏性气道炎症可以独立于可检测到的特异性抗体。此外，取决于致敏途径，AHR可以由IL-4 / IL-13或IFN-γ诱导。

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