Journal
FEMS MICROBIOLOGY REVIEWS
Volume 42, Issue 5, Pages 656-671Publisher
OXFORD UNIV PRESS
DOI: 10.1093/femsre/fuy025
Keywords
Staphylococcus aureus; pattern recognition receptors; inflammatory responses; evasion; virulence; biotherapeutic
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Funding
- Northern Norway Regional Health Authority [Helse Nord RHF] [SFP1231-15]
- U.S. National Institutes of Health [U01 AI124316, R01 HL125352]
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL125352] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [U01AI124316] Funding Source: NIH RePORTER
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Early recognition of pathogens by the innate immune system is crucial for bacterial clearance. Many pattern recognition receptors (PRRs) such as Toll-like (TLRs) and (NOD)-like (NLRs) receptors have been implicated in initial sensing of bacterial components. The intracellular signaling cascades triggered by these receptors result in transcriptional upregulation of inflammatory pathways. Although this step is crucial for bacterial elimination, it is also associated with the potential for substantial immunopathology, which underscores the need for tight control of inflammatory responses. The leading human bacterial pathogen Staphylococcus aureus expresses over 100 virulence factors that exert numerous effects upon host cells. In this manner, the pathogen seeks to avoid host recognition or perturb PRR-induced innate immune responses to allow optimal survival in the host. These immune system interactions may result in enhanced bacterial proliferation but also provoke systemic cytokine responses associated with sepsis. This review summarizes recent findings on the various mechanisms applied by S. aureus to modulate or interfere with inflammatory responses through PRRs. Detailed understanding of these complex interactions can provide new insights toward future immune-stimulatory therapeutics against infection or immunomodulatory therapeutics to suppress or correct dysregulated inflammation.
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