Journal
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 103, Issue 37, Pages 13831-13836Publisher
NATL ACAD SCIENCES
DOI: 10.1073/pnas.0603072103
Keywords
innate immunity; virulence
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Funding
- NIAID NIH HHS [AI055838, R03 AI055838] Funding Source: Medline
- NICHD NIH HHS [K12-HD00850, K12 HD000850] Funding Source: Medline
- NIGMS NIH HHS [T32GM007183, T32 GM007183] Funding Source: Medline
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Toll-like receptors and other immune-signaling pathways play important roles as sensors of bacterial pattern molecules, such as peptidoglycan, lipoprotein, or teichoic acid, triggering innate host immune responses that prevent infection. Immune recognition of multiple bacterial products has been viewed as a safeguard against stealth infections; however, this hypothesis has never been tested for Staphylococcus aureus, a frequent human pathogen. By generating mutations that block the diacylglycerol modification of lipoprotein precursors, we show here that S. aureus variants lacking lipoproteins escape immune recognition and cause lethal infections with disseminated abscess formation, failing to elicit an adequate host response. Thus, lipoproteins appear to play distinct, nonredundant roles in pathogen recognition and host innate defense mechanisms against S. aureus infections.
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