Increased susceptibility to bacterial superinfection as a consequence of innate antiviral responses.
- Navarini AA Institute for Experimental Immunology, University Hospital Zurich, Schmelzbergstrasse 12, CH-8091 Zurich, Switzerland. navarini@hotmail.com
- Recher M
- Lang KS
- Georgiev P
- Meury S
- Bergthaler A
- Flatz L
- Bille J
- Landmann R
- Odermatt B
- Hengartner H
- Zinkernagel RM
- 2006-10-13
Published in:
- 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
English
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.
- Language
-
- English
- Open access status
- bronze
- Identifiers
-
- DOI 10.1073/pnas.0607325103
- PMID 17030789
- Persistent URL
- https://sonar.ch/global/documents/4238
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