Navarini AA Recher M Lang KS Georgiev P Meury S Bergthaler A Flatz L Bille J Landmann R Odermatt B Hengartner H Zinkernagel RM 2006 The reason why severe localized or systemic virus infections enhance and aggravate bacterial superinfection is poorly understood. Here we show that virus-induced IFN type I caused apoptosis in bone marrow granulocytes, drastically reduced granulocyte infiltrates at the site of bacterial superinfection, caused up to 1,000-fold higher bacterial titers in solid organs, and increased disease susceptibility. The finding that the innate antiviral immune response reduces the antibacterial granulocyte defense offers an explanation for enhanced susceptibility to bacterial superinfection during viral disease. application/pdf https://sonar.ch/global/documents/4238 eng info:eu-repo/semantics/altIdentifier/doi/10.1073/pnas.0607325103 info:eu-repo/semantics/altIdentifier/pmid/17030789 info:eu-repo/semantics/openAccess Proceedings of the National Academy of Sciences of the United States of America. - 2006 Agranulocytosis Animals Apoptosis Bacterial Infections Bone Marrow Cells Disease Susceptibility Granulocytes Immunity, Innate Interferon Type I Listeria monocytogenes Liver Lymphocytic Choriomeningitis Lymphocytic choriomeningitis virus Mice Mice, Inbred C57BL Mice, Knockout Receptor, Interferon alpha-beta Spleen Staphylococcus aureus Superinfection Virus Diseases Increased susceptibility to bacterial superinfection as a consequence of innate antiviral responses. http://purl.org/coar/resource_type/c_6501