Type I interferon does not promote susceptibility to foodborne Listeria monocytogenes

• Published in: The Journal of immunology (1950) Vol. 196; no. 7; pp. 3109 - 3116
• Main Authors: Pitts, Michelle G., Myers-Morales, Tanya, D’Orazio, Sarah E.F.
• Format: Journal Article
• Language: English
• Published: 19.02.2016
• ISSN: 0022-1767; 1550-6606
• DOI: 10.4049/jimmunol.1502192

Type I IFN (IFNα/β) is thought to enhance growth of the foodborne intracellular pathogen Listeria monocytogenes ( Lm ) by promoting mechanisms that dampen innate immunity to infection. However, the type I IFN response has been studied primarily using methods that bypass the stomach and, therefore, fail to replicate the natural course of Lm infection. In this study, we compared i.v. and foodborne transmission of Lm in mice lacking the common type I IFN receptor (IFNAR1 −/− ). Contrary to what was observed using i.v. infection, IFNAR1 −/− and wild type mice had similar bacterial burdens in the liver and spleen following foodborne infection. Splenocytes from wild type mice infected intravenously produced significantly more IFNβ than those infected by the foodborne route. Consequently, the immunosuppressive effects of type I IFN signaling, which included T cell death, increased IL-10 secretion, and repression of neutrophil recruitment to the spleen, were all observed following i.v., but not foodborne transmission of Lm . Type I IFN was also previously shown to cause a loss of responsiveness to IFNγ through down-regulation of the receptor IFNGR1 on macrophages and dendritic cells. However, we detected a decrease in surface expression of IFNGR1 even in the absence of IFNα/β signaling, suggesting that in vivo, this infection-induced phenotype is not type I IFN-dependent. These results highlight the importance of using the natural route of infection for studies of host-pathogen interactions and suggest that the detrimental effects of IFNα/β signaling on the innate immune response to Lm may be an artifact of the i.v. infection model.