| Literature DB >> 25395539 |
Benyue Zhang1, Benoit Chassaing1, Zhenda Shi1, Robin Uchiyama2, Zhan Zhang1, Timothy L Denning2, Sue E Crawford3, Andrea J Pruijssers4, Jason A Iskarpatyoti4, Mary K Estes3, Terence S Dermody5, Wenjun Ouyang6, Ifor R Williams7, Matam Vijay-Kumar8, Andrew T Gewirtz9.
Abstract
Activators of innate immunity may have the potential to combat a broad range of infectious agents. We report that treatment with bacterial flagellin prevented rotavirus (RV) infection in mice and cured chronically RV-infected mice. Protection was independent of adaptive immunity and interferon (IFN, type I and II) and required flagellin receptors Toll-like receptor 5 (TLR5) and NOD-like receptor C4 (NLRC4). Flagellin-induced activation of TLR5 on dendritic cells elicited production of the cytokine interleukin-22 (IL-22), which induced a protective gene expression program in intestinal epithelial cells. Flagellin also induced NLRC4-dependent production of IL-18 and immediate elimination of RV-infected cells. Administration of IL-22 and IL-18 to mice fully recapitulated the capacity of flagellin to prevent or eliminate RV infection and thus holds promise as a broad-spectrum antiviral agent.Entities:
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Year: 2014 PMID： 25395539 PMCID： PMC4788408 DOI： 10.1126/science.1256999
Source DB: PubMed Journal: Science ISSN： 0036-8075 Impact factor: 47.728