ArticleNature medicine2009
Commensal bacteria regulate Toll-like receptor 3-dependent inflammation after skin injury.
Article in Nature medicine, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 391 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
391 citing papers in PubMed, 1 synthesis or guideline pooled it, 762 citations in OpenAlex.
- Pathogenic characterization and drug resistance of neonatal sepsis in China: a systematic review and meta-analysis.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2025Pooled it
- Chlorhexidine vs Routine Foot Washing to Prevent Diabetic Foot Ulcers: A Randomized Clinical Trial.JAMA network open · 2025Trial
- Immune silencing by a lipid virulence factor of Staphylococcus.Communications biology · 2026Article
- Keratinocytes: A key player in skin immunity and their emerging roles in secondary lymphedema.JID innovations : skin science from molecules to population health · 2026Review
- Review
- Microbiome-Driven Bioactives for Chronic Wound Repair: Microbial Metabolites, Host-Microbe Mechanisms and Paths to Clinical Translation.Molecules (Basel, Switzerland) · 2026Review
- Synergistic tissue destruction byBiofilm · 2026Article
- NLRP1 inflammasome activation in skin equivalents reveals mechanistic insights into the roles of keratinocytes in psoriasis.Cell death & disease · 2026Article
- Beyond Inflammation: The Role of Oxidative Stress and Gut-Skin Axis Dysbiosis in the Pathogenesis of Immune-Mediated Skin Disorders and Potential Therapeutic Implications.International journal of molecular sciences · 2026Review
- Oxygen and ROS Delivery for Infected Wound Healing and Future Prospects.Advanced healthcare materials · 2026Review
- Staphylococcus aureus in atopic dermatitis: How a common bacterium exploits and drives disease.The Journal of allergy and clinical immunology · 2026Review
- Human keratinocytes exhibit limited potential for SARS-CoV-2 infection despite ACE2 and mature cathepsin L expression.JID innovations : skin science from molecules to population health · 2026Article
- New concept in wound infection management: From bacterial eradication to microbiome modulation.APL bioengineering · 2026Article
- Atopic Dermatitis-like mouse model using early inoculation of patient-derivedJID innovations : skin science from molecules to population health · 2026Article
- Interplay of Microbiome, Oxidative Stress and Inflammation in Health and Disease.Antioxidants (Basel, Switzerland) · 2026Review
- Article
- Article
- Dynamic remodeling of skin microbiota during healthy homeostatic and wound repair conditions.Frontiers in microbiology · 2026Review
- The challenges and strategies for navigatingTheranostics · 2026Review
- The Scalp Microbiome-Hair Axis: Mechanisms and Therapeutic Translation.Research (Washington, D.C.) · 2026Review
331 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
14 authors at 5 institutions in 3 countries.
Funding
Abstract
The normal microflora of the skin includes staphylococcal species that will induce inflammation when present below the dermis but are tolerated on the epidermal surface without initiating inflammation. Here we reveal a previously unknown mechanism by which a product of staphylococci inhibits skin inflammation. This inhibition is mediated by staphylococcal lipoteichoic acid (LTA) and acts selectively on keratinocytes triggered through Toll-like receptor 3(TLR3). We show that TLR3 activation is required for normal inflammation after injury and that keratinocytes require TLR3 to respond to RNA from damaged cells with the release of inflammatory cytokines. Staphylococcal LTA inhibits both inflammatory cytokine release from keratinocytes and inflammation triggered by injury through a TLR2-dependent mechanism. To our knowledge, these findings show for the first time that the skin epithelium requires TLR3 for normal inflammation after wounding and that the microflora can modulate specific cutaneous inflammatory responses.
Indexed as
Identifiers
What OpenQuestion holds
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.