ReviewClinical microbiology reviews2005
Recognition of Staphylococcus aureus by the innate immune system.
Review in Clinical microbiology reviews, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 215 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
215 citing papers in PubMed, 1 synthesis or guideline pooled it, 472 citations in OpenAlex.
- Host-Bacterium Interaction Mechanisms inInternational journal of molecular sciences · 2023Pooled it
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- A comprehensive review of emerging therapeutic strategies against methicillin-resistantFrontiers in microbiology · 2026Review
- In Vitro Analysis of the Dynamic Role of the Bacterial Virulence Factors in Skin Wound Healing.International journal of molecular sciences · 2025Article
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- Mechanisms of microbial infection and wound healing in diabetic foot ulcer: pathogenicity in the inflammatory-proliferative phase, chronicity, and treatment strategies.Frontiers in endocrinology · 2025Review
- Bacterial and host interactions inFrontiers in microbiology · 2025Review
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- Bacteria-activated macrophage membrane coated ROS-responsive nanoparticle for targeted delivery of antibiotics to infected wounds.Journal of nanobiotechnology · 2024Article
- Investigating the Antibiotic Resistance Pattern of MRSA in Cancer Patients.Archives of Razi Institute · 2024Article
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- Regulation of Airway Epithelial-Derived Alarmins in Asthma: Perspectives for Therapeutic Targets.Biomedicines · 2024Review
155 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The gram-positive bacterium Staphylococcus aureus is a major pathogen responsible for a variety of diseases ranging from minor skin infections to life-threatening conditions such as sepsis. Cell wall-associated and secreted proteins (e.g., protein A, hemolysins, and phenol-soluble modulin) and cell wall components (e.g., peptidoglycan and alanylated lipoteichoic acid) have been shown to be inflammatory, and these staphylococcal components may contribute to sepsis. On the host side, many host factors have been implicated in the innate detection of staphylococcal components. One class of pattern recognition molecules, Toll-like receptor 2, has been shown to function as the transmembrane component involved in the detection of staphylococcal lipoteichoic acid and phenol-soluble modulin and is involved in the synthesis of inflammatory cytokines by monocytes/macrophages in response to these components. Nod2 (nucleotide-binding oligomerization domain 2) is the intracellular sensor for muramyl dipeptide, the minimal bioactive structure of peptidoglycan, and it may contribute to the innate immune defense against S. aureus. The staphylococcal virulence factor protein A was recently shown to interact directly with tumor necrosis factor receptor 1 in airway epithelium and to reproduce the effects of tumor necrosis factor alpha. Finally, peptidoglycan recognition protein L is an amidase that inactivates the proinflammatory activities of peptidoglycan. However, peptidoglycan recognition protein L probably plays a minor role in the innate immune response to S. aureus. Thus, several innate immunity receptors may be implicated in host defense against S. aureus.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.