ILC2s mediate systemic innate protection by priming mucus production at distal mucosal sites

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.

Source: The Journal of Experimental Medicine - December 1, 2019 Category: Internal Medicine Authors: Campbell, L., Hepworth, M. R., Whittingham-Dowd, J., Thompson, S., Bancroft, A. J., Hayes, K. S., Shaw, T. N., Dickey, B. F., Flamar, A.-L., Artis, D., Schwartz, D. A., Evans, C. M., Roberts, I. S., Thornton, D. J., Grencis, R. K. Tags: Innate Immunity and Inflammation, Infectious Disease and Host Defense, Mucosal Immunology Brief Definitive Reports Source Type: research