Lambda Interferon Restructures the Nasal Microbiome and Increases Susceptibility to Staphylococcus aureus Superinfection

• DOI: 10.1128/mbio.01939-15
• Publication Date: 2016-02-10T02:50:22Z
• Authors: Paul J. Planet; Dane Parker; Taylor S. Cohen; Hannah Smith; Justinne D. Leon; Chanelle Ryan; Tobin J. Hammer; Noah Fierer; Emily I. Chen; Alice S. Prince
• Keywords: Superinfection

Much of the morbidity and mortality associated with influenza virus respiratory infection is due to bacterial coinfection pathogens that colonize upper tract such as methicillin-resistant Staphylococcus aureus (MRSA) Streptococcus pneumoniae. A major component immune response production type I III interferons. Here we show causes an increase restructuring microbiota in wild-type (WT) mice but not Il28r(-/-) mutant lacking receptor for interferon. Mice IL-28 fail induce STAT1 phosphorylation expression its regulator, SOCS1. have increased interleukin-22 (IL-22), well Ngal RegIIIγ, nasal cavity, source organisms would be aspirated cause pneumonia. Proteomic analysis reveals changes several cytoskeletal proteins contribute barrier function epithelium may effects signaling on microbiota. The importance pathogenesis MRSA pneumonia after was confirmed by showing WT nasally colonized before or had significantly higher levels airways, greater susceptibility than did. Our results suggest activation interferon has a effect expanding airway microbiome increasing lower infection.S. are important pathogens, these significant mortality. ability S. less understood. We here leads change interferon-dependent manner. altered IL-22 signaling. In studies, without colonization subsequent infected This work demonstrates interferons induced superinfection.