NDLI: Failure to induce IFN-ß production during Staphylococcus aureus infection contributes to pathogenicity.

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Failure to induce IFN-ß production during Staphylococcus aureus infection contributes to pathogenicity.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Kaplan, Amber Liu, George Y. Underhill, David M. Tseng, Ching Wen Ma, Jun Becker, Courtney A. Wolf, Andrea J. Kyme, Pierre
Description	Country affiliation: United States Author Affiliation: Kaplan A ( Inflammatory Bowel and Immunobiology Research Institute, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA.)
Abstract	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-ß production in myeloid cells, but this IFN-ß is not always beneficial to the host. We examined whether Staphylococcus aureus induces IFN-ß 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-ß 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-ß and inflammatory chemokines downstream of IFN-ß. Further, we found that adding exogenous IFN-ß during S. aureus infection (in vitro and in vivo) was protective. Together, the data demonstrate that failure to induce IFN-ß production during S. aureus infection contributes to pathogenicity.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1201111
Journal	The Journal of Immunology
Issue Number	9
Volume Number	189
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2012-11-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Interferon-beta Staphylococcal Infections Immunology Microbiology Staphylococcus Aureus Pathogenicity Animals Cells, Cultured Disease Models, Animal Antagonists & Inhibitors Biosynthesis Genetics Mice Mice, Inbred C57bl Mice, Knockout Mutation Blood Research Support, N.i.h., Extramural Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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