Journal
JOURNAL OF IMMUNOLOGY
Volume 207, Issue 1, Pages 257-267Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.2001304
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Funding
- Foundation for the National Institutes of Health [R01 AI138203, R01 AI109317-05, P20 GM113123]
- University of North Dakota [P20 GM103442, 5P20 GM113123]
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The gut microbiota plays a vital role in regulating the migration of ILC2 cells through the gut-lung axis, influencing host defense against infection. The study shows that two types of ILC2 cells have distinct but crucial roles in host immunity.
Gut microbiota is increasingly linked to the development of various pulmonary diseases through a gut-lung axis. However, the mechanisms by which gut commensal microbes impact trafficking and functional transition of immune cells remain largely unknown. Using integrated microbiota dysbiosis approaches, we uncover that the gut microbiota directs the migration of group 2 innate lymphoid cells (ILC2s) from the gut to the lung through a gut-lung axis. We identify Proteobacteria as a critical species in the gut microbiome to facilitate natural ILC2 migration, and increased Proteobacteria induces IL-33 production. Mechanistically, IL-33-CXCL16 signaling promotes the natural ILC2 accumulation in the lung, whereas IL-25-CCL25 signals augment inflammatory ILC2 accumulation in the intestines upon abdominal infection, parabiosis, and cecum ligation and puncture in mice. We reveal that these two types of ILC2s play critical but distinct roles in regulating inflammation, leading to balanced host defense against infection. Overall results delineate that Proteobacteria in gut microbiota modulates ILC2 directional migration to the lung for host defense via regulation of select cytokines (IL-33), suggesting novel therapeutic strategies to control infectious diseases.
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