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Intestinal helminth infection promotes IL-5- and CD4+ T cell-dependent immunity in the lung against migrating parasites.
Mucosal Immunology ( IF 7.9 ) Pub Date : 2018-Nov-06 , DOI: 10.1038/s41385-018-0102-8 Kara J Filbey 1 , Mali Camberis 1 , Jodie Chandler 1 , Rufus Turner 2 , Anthony J Kettle 2 , Ramon M Eichenberger 3 , Paul Giacomin 3 , Graham Le Gros 1
Mucosal Immunology ( IF 7.9 ) Pub Date : 2018-Nov-06 , DOI: 10.1038/s41385-018-0102-8 Kara J Filbey 1 , Mali Camberis 1 , Jodie Chandler 1 , Rufus Turner 2 , Anthony J Kettle 2 , Ramon M Eichenberger 3 , Paul Giacomin 3 , Graham Le Gros 1
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The ability of helminths to manipulate the immune system of their hosts to ensure their own survival is often credited with affecting responses to other pathogens. We undertook co-infection experiments in mice to determine how infection with the intestinal helminth Heligmosomoides polygyrus affected the parasitological, immunological and physiological outcomes of a primary infection with a distinct species of helminth; the lung migratory parasite Nippostrongylus brasiliensis. We found that migrating N. brasiliensis larvae were killed in the lungs of H. polygyrus-infected mice by a process involving IL-33-activated CD4+ T cells that released IL-5 and recruited activated eosinophils. The lung pathology normally associated with N. brasiliensis larval migration was also reduced. Importantly, lung immunity remained intact in mice cleared of prior H. polygyrus infection and also occurred during infection with another entirely enteric helminth, Trichuris muris. This study identifies a cross-mucosal immune mechanism by which intestinal helminths may protect their hosts against co-infection by a different parasite at a distal site, via circulation of activated CD4+ T cells that can be triggered to release effector cytokines and mount inflammatory responses by tissue damage-associated alarmins, such as IL-33.
中文翻译：
肠道蠕虫感染可促进肺部 IL-5 和 CD4+ T 细胞依赖性免疫力抵抗迁移寄生虫。
蠕虫操纵宿主免疫系统以确保自身生存的能力通常被认为会影响对其他病原体的反应。我们在小鼠身上进行了合并感染实验，以确定肠道蠕虫 Heligmosomoides polygyrus 的感染如何影响不同种类蠕虫原发感染的寄生虫学、免疫学和生理学结果；肺迁移性寄生虫 Nippostrongylus brasiliensis。我们发现迁移的 N. brasiliensis 幼虫在 H. polygyrus 感染小鼠的肺部被 IL-33 激活的 CD4 +杀死释放 IL-5 并募集活化嗜酸性粒细胞的 T 细胞。通常与巴西橡胶树幼虫迁移相关的肺部病理学也有所减少。重要的是，在清除了之前多回嗜血杆菌感染的小鼠中，肺免疫力仍然完好无损，并且在感染另一种完全肠道蠕虫鼠鞭虫时也会发生。这项研究确定了一种跨粘膜免疫机制，通过该机制，肠道蠕虫可以保护宿主免受远端部位不同寄生虫的共同感染，通过激活的 CD4 + T 细胞循环，这些细胞可以被触发释放效应细胞因子并产生炎症反应通过组织损伤相关的警报，如 IL-33。
更新日期：2019-01-26
中文翻译：
肠道蠕虫感染可促进肺部 IL-5 和 CD4+ T 细胞依赖性免疫力抵抗迁移寄生虫。
蠕虫操纵宿主免疫系统以确保自身生存的能力通常被认为会影响对其他病原体的反应。我们在小鼠身上进行了合并感染实验，以确定肠道蠕虫 Heligmosomoides polygyrus 的感染如何影响不同种类蠕虫原发感染的寄生虫学、免疫学和生理学结果；肺迁移性寄生虫 Nippostrongylus brasiliensis。我们发现迁移的 N. brasiliensis 幼虫在 H. polygyrus 感染小鼠的肺部被 IL-33 激活的 CD4 +杀死释放 IL-5 并募集活化嗜酸性粒细胞的 T 细胞。通常与巴西橡胶树幼虫迁移相关的肺部病理学也有所减少。重要的是，在清除了之前多回嗜血杆菌感染的小鼠中，肺免疫力仍然完好无损，并且在感染另一种完全肠道蠕虫鼠鞭虫时也会发生。这项研究确定了一种跨粘膜免疫机制，通过该机制，肠道蠕虫可以保护宿主免受远端部位不同寄生虫的共同感染，通过激活的 CD4 + T 细胞循环，这些细胞可以被触发释放效应细胞因子并产生炎症反应通过组织损伤相关的警报，如 IL-33。
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