ArticleBlood2006
The extracellular adherence protein (Eap) of Staphylococcus aureus inhibits wound healing by interfering with host defense and repair mechanisms.
Article in Blood, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
What it found
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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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Who cites it
43 citing papers in PubMed, 107 citations in OpenAlex.
- Methicillin-resistant Staphylococcus aureus.Nature reviews. Disease primers · 2026Review
- Prevalence and Mechanisms of Itch in Chronic Wounds: A Narrative Review.Journal of clinical medicine · 2025Review
- Implant-DerivedAntibiotics (Basel, Switzerland) · 2025Article
- Staphylococcus aureus vesicles impair cutaneous wound healing through p38 MAPK-MerTK cleavage-mediated inhibition of macrophage efferocytosis.Cell communication and signaling : CCS · 2025Article
- Iron Metabolism of the Skin: Recycling versus Release.Metabolites · 2023Review
- Protein Disulfide Isomerase and Extracellular Adherence Protein Cooperatively Potentiate Staphylococcal Invasion into Endothelial Cells.Microbiology spectrum · 2023Article
- Garlic and ginger essential oil-based neomycin nano-emulsions as effective and accelerated treatment for skin wounds' healing and inflammation:Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2022Article
- The potential action of SSRIs in the treatment of skin diseases including atopic dermatitis and slow-healing wounds.Pharmacological reports : PR · 2022Review
- Article
- Virulence factors and clonal diversity of Staphylococcus aureus in colonization and wound infection with emphasis on diabetic foot infection.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2020Review
- Review
- Encapsulation of collagen mimetic peptide-tethered vancomycin liposomes in collagen-based scaffolds for infection control in wounds.Acta biomaterialia · 2020Article
- Vascular endothelial Cdc42 deficiency delays skin wound-healing processes by increasing IL-1β and TNF-α expression.American journal of translational research · 2019Article
- Staphylococcus aureus colonization and non-influenza respiratory viruses: Interactions and synergism mechanisms.Virulence · 2018Review
- TheFrontiers in cellular and infection microbiology · 2018Article
- Role of SCCmec type in resistance to the synergistic activity of oxacillin and cefoxitin in MRSA.Scientific reports · 2017Article
- Endogenous developmental endothelial locus-1 limits ischaemia-related angiogenesis by blocking inflammation.Thrombosis and haemostasis · 2017Article
- Shaping of cutaneous function by encounters with commensals.The Journal of physiology · 2017Review
- An Update on Clinical Burden, Diagnostic Tools, and Therapeutic Options ofInfectious diseases · 2017Review
- Novel Evasion Mechanisms of the Classical Complement Pathway.Journal of immunology (Baltimore, Md. : 1950) · 2016Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
16 authors at 1 institution in 2 countries.
Funding
Abstract
Staphylococcus aureus is a major human pathogen interfering with host-cell functions. Impaired wound healing is often observed in S aureus-infected wounds, yet, the underlying mechanisms are poorly defined. Here, we identify the extracellular adherence protein (Eap) of S aureus to be responsible for impaired wound healing. In a mouse wound-healing model wound closure was inhibited in the presence of wild-type S aureus and this effect was reversible when the wounds were incubated with an isogenic Eap-deficient strain. Isolated Eap also delayed wound closure. In the presence of Eap, recruitment of inflammatory cells to the wound site as well as neovascularization of the wound were prevented. In vitro, Eap significantly reduced intercellular adhesion molecule 1 (ICAM-1)-dependent leukocyte-endothelial interactions and diminished the consequent activation of the proinflammatory transcription factor nuclear factor kappaB (NFkappaB) in leukocytes associated with a decrease in expression of tissue factor. Moreover, Eap blocked alphav-integrin-mediated endothelial-cell migration and capillary tube formation, and neovascularization in matrigels in vivo. Collectively, the potent anti-inflammatory and antiangiogenic properties of Eap provide an underlying mechanism that may explain the impaired wound healing in S aureus-infected wounds. Eap may also serve as a lead compound for new anti-inflammatory and antiangiogenic therapies in several pathologies.
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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.