Journal
CELL HOST & MICROBE
Volume 17, Issue 1, Pages 85-97Publisher
CELL PRESS
DOI: 10.1016/j.chom.2014.11.004
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Funding
- NIH [DK071619, AI08488702, P50CA94056, AI080672, AR048335, AI056160]
- CCFA Genetics Consortium
- Shawn Hu and Angela Zeng Graduate Fellowship
- National Institute of Diabetes and Digestive and Kidney Disease (NIDDK) [P30DK052574]
- NCI Cancer Center Support Grant [P30CA91842]
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The host immune system functions constantly to maintain chronic commensal and pathogenic organisms in check. The consequences of these immune responses on host physiology are as yet unexplored, and may have long-term implications in health and disease. We show that chronic viral infection increases epithelial turnover in multiple tissues, and the antiviral cytokines type I interferons (IFNs) mediate this response. Using a murine model with persistently elevated type I IFNs in the absence of exogenous viral infection, the Irgm1(-/-) mouse, we demonstrate that type I IFNs act through nonepithelial cells, including macrophages, to promote increased epithelial turnover and wound repair. Downstream of type I IFN signaling, the highly related IFN-stimulated genes Apolipoprotein L9a and b activate epithelial proliferation through ERK activation. Our findings demonstrate that the host immune response to chronic viral infection has systemic effects on epithelial turnover through a myeloidepithelial circuit.
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