Journal
JOURNAL OF EXPERIMENTAL MEDICINE
Volume 216, Issue 12, Pages 2714-2723Publisher
ROCKEFELLER UNIV PRESS
DOI: 10.1084/jem.20180610
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Funding
- Biotechnology and Biological Sciences Research Council
- Wellcome Trust [0836202, 210661, 203128/Z/16/Z]
- University of Manchester Strategic Fund
- Wellcome Trust Institutional Strategic Support Fund [105610]
- Wellcome Trust/Royal Society Sir Henry Dale Fellowship Award [105644/Z/14/Z]
- Lister Institute of Preventive Medicine Research Fellowship
- Royal Society Wolfson Research Merit Award
- Wellcome Trust [105644/Z/14/Z] Funding Source: Wellcome Trust
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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.
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