Host immunity to parasitic nematodes requires the generation of a robust type 2 cytokine response, characterized by the production of interleukin 13 (IL-13), which drives expulsion. Here, we show that infection with helminths in the intestine also induces an ILC2-driven, IL-13-dependent goblet cell hyperplasia and increased production of mucins (Muc5b and Muc5ac) at distal sites, including the lungs and other mucosal barrier sites. Critically, we show that type 2 priming of lung tissue through increased mucin production inhibits the progression of a subsequent lung migratory helminth infection and limits its transit through the airways. These data show that infection by gastrointestinal-dwelling helminths induces a systemic innate mucin response that primes peripheral barrier sites for protection against subsequent secondary helminth infections. These data suggest that innate-driven priming of mucus barriers may have evolved to protect from subsequent infections with multiple helminth species, which occur naturally in endemic areas.

中文翻译：

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ILC2 通过在远端粘膜部位引发粘液产生来介导系统性先天保护。

宿主对寄生线虫的免疫需要产生强大的 2 型细胞因子反应，其特征是产生白细胞介素 13 (IL-13)，从而驱动排出。在这里，我们发现肠道中的蠕虫感染也会诱导 ILC2 驱动的、IL-13 依赖性杯状细胞增生，并在远端部位（包括肺和其他粘膜屏障部位）增加粘蛋白（Muc5b 和 Muc5ac）的产生。至关重要的是，我们表明，通过增加粘蛋白产生而引发的 2 型肺组织抑制了随后的肺迁移性蠕虫感染的进展，并限制了其通过气道的转运。这些数据表明，胃肠道蠕虫感染会引发全身性先天性粘蛋白反应，从而启动外周屏障部位以防止随后的继发性蠕虫感染。