Document Type
Article
Language
eng
Format of Original
13 p.
Publication Date
1-2015
Publisher
Elsevier
Source Publication
Cell Host & Microbe
Source ISSN
1931-3128
Abstract
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 myeloid-epithelial circuit.
Recommended Citation
Sun, Lulu; Miyoshi, Hiroyuki; Origanti, Sofia; Nice, Timothy J.; Barger, Alexandra C.; Manieri, Nicholas A.; Fogel, Leslie A.; French, Anthony R.; Piwnica-Worms, David; Piwnica-Worms, Helen; Virgin, Herbert W.; Lenschow, Deborah J.; and Stappenbeck, Thaddeus S., "Type I Interferons Link Viral Infection to Enhanced Epithelial Turnover and Repair" (2015). Biological Sciences Faculty Research and Publications. 431.
https://epublications.marquette.edu/bio_fac/431
Comments
Accepted version. Cell Host & Microbe, Vol. 17, No. 1 (January 2015): 85-97. DOI. © Elsevier (Cell Press). Used with permission.
Sofia Origanti was affiliated with Washington University School of Medicine at the time of publication.