Type I Interferon Signaling Regulates Ly6Chi Monocytes and Neutrophils during Acute Viral Pneumonia in Mice

• DOI: 10.1371/journal.ppat.1001304
• Publication Date: 2011-02-24T21:43:15Z
• Authors: Sang-Uk Seo; Hyung-Joon Kwon; Hyun-Jeong Ko; Young-Ho Byun; Baik Lin Seong; Satoshi Uematsu; Shizuo Akira; Mi-Na Kweon
• Keywords: Monocyte

Type I interferon (IFN-I) plays a critical role in the homeostasis of hematopoietic stem cells and influences neutrophil influx to site inflammation. IFN-I receptor knockout (Ifnar1−/−) mice develop significant defects infiltration Ly6Chi monocytes lung after influenza infection (A/PR/8/34, H1N1). wild-type (WT) are main producers MCP-1 while alternatively generated Ly6Cint Ifnar1−/− mainly produce KC for influx. As consequence, recruit more neutrophils than do WT mice. Treatment IFNAR1 blocking antibody on bone marrow (BM) vitro failed differentiate into monocytes. By using BM chimeric (WT vice versa), we confirmed that signaling is required generation Of note, reconstituted with increased numbers survived longer influenza-infected In contrast, received alternative exhibited higher mortality rates given cells. Collectively, these data suggest contributes resistance by control lung.