Failure to induce interferon-beta production during Staphylococcus aureus infection contributes to pathogenicity
| Autor: | Pierre Kyme, Jun Ma, Ching Wen Tseng, Andrea J. Wolf, Amber T. Kaplan, David M. Underhill, Courtney A. Becker, George Y. Liu |
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| Jazyk: | angličtina |
| Rok vydání: | 2012 |
| Předmět: |
Chemokine
Staphylococcus aureus Myeloid Immunology Mutant medicine.disease_cause Article Microbiology Mice In vivo medicine Immunology and Allergy Animals Humans Cells Cultured Phagosome Mice Knockout biology Interferon-beta Staphylococcal Infections biology.organism_classification In vitro Mice Inbred C57BL Disease Models Animal medicine.anatomical_structure Mutation biology.protein Bacteria |
| Popis: | The importance of type I IFNs in the host response to viral infection is well established; however, their role in bacterial infection is not fully understood. Several bacteria (both Gram-positive and -negative) have been shown to induce IFN-β production in myeloid cells, but this IFN-β is not always beneficial to the host. We examined whether Staphylococcus aureus induces IFN-β from myeloid phagocytes, and if so, whether it is helpful or harmful to the host to do so. We found that S. aureus poorly induces IFN-β production compared with other bacteria. S. aureus is highly resistant to degradation in the phagosome because it is resistant to lysozyme. Using a mutant that is more sensitive to lysozyme, we show that phagosomal degradation and release of intracellular ligands is essential for induction of IFN-β and inflammatory chemokines downstream of IFN-β. Further, we found that adding exogenous IFN-β during S. aureus infection (in vitro and in vivo) was protective. Together, the data demonstrate that failure to induce IFN-β production during S. aureus infection contributes to pathogenicity. |
| Databáze: | OpenAIRE |
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