ReviewExperimental dermatology2021
Intracellular escape strategies of Staphylococcus aureus in persistent cutaneous infections.
Review in Experimental dermatology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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
23 citing papers in PubMed, 44 citations in OpenAlex.
- Gelatinase regulates the egress of intracellular replicating populations during Enterococcus faecalis infection.PLoS pathogens · 2026Article
- Antibacterial Immunotherapy: Mechanistic Insights, Emerging Therapeutic Strategies, and Clinical Translation.Infection and drug resistance · 2026Review
- Postbiotics as microbial-derived therapeutics for wound healing disorders: from molecular mechanisms to future application.Cell communication and signaling : CCS · 2025Review
- Comprehensive biological evaluation of infuzide as a potent antimicrobial, alone and in combination with gentamicin, linezolid, and minocycline targeting MDRMicrobiology spectrum · 2025Article
- Antibacterial Evaluation of Tricyclic Antidepressants AgainstPathogens (Basel, Switzerland) · 2025Article
- The epidermal lipid-microbiome loop and immunity: Important players in atopic dermatitis.Journal of advanced research · 2025Review
- Tissue resident cells differentiate S. aureus from S. epidermidis via IL-1β following barrier disruption in healthy human skin.PLoS pathogens · 2024Article
- Postbiotic lactobacilli induce cutaneous antimicrobial response and restore the barrier to inhibit the intracellular invasion of Staphylococcus aureus in vitro and ex vivo.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024Article
- The phosphatidylinositol-5' phosphatase synaptojanin1 limits integrin-mediated invasion ofMicrobiology spectrum · 2024Article
- Identification of kinase modulators as host-directed therapeutics against intracellular methicillin-resistantFrontiers in cellular and infection microbiology · 2024Article
- Immunomodulatory biomaterials against bacterial infections: Progress, challenges, and future perspectives.Innovation (Cambridge (Mass.)) · 2023Review
- Review
- PEI-PLGA nanoparticles significantly enhanced the immunogenicity of IsdBImmunity, inflammation and disease · 2023Article
- Longitudinal study of wound healing status and bacterial colonisation of Staphylococcus aureus and Corynebacterium diphtheriae in epidermolysis bullosa patients.International wound journal · 2023Article
- Microbiome dysbiosis occurred in hypertrophic scars is dominated byFrontiers in immunology · 2023Article
- Atopic dermatitis-derivedFrontiers in cellular and infection microbiology · 2023Article
- T-cell activation and bacterial infection in skin wounds of recessive dystrophic epidermolysis bullosa patients.Experimental dermatology · 2022Article
- Advanced Wound Diagnostics: Toward Transforming Wound Care into Precision Medicine.Advances in wound care · 2022Review
- The Influence of Antibiotic Resistance on Innate Immune Responses toAntibiotics (Basel, Switzerland) · 2022Review
- Non-Canonical Host Intracellular Niche Links to New Antimicrobial Resistance Mechanism.Pathogens (Basel, Switzerland) · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Pathogenic invasion of Staphylococcus aureus is a major concern in patients with chronic skin diseases like atopic dermatitis (AD), epidermolysis bullosa (EB), or chronic diabetic foot and venous leg ulcers, and can result in persistent and life-threatening chronic non-healing wounds. Staphylococcus aureus is generally recognized as extracellular pathogens. However, S. aureus can also invade, hide and persist in skin cells to contribute to wound chronicity. The intracellular life cycle of S. aureus is currently incompletely understood, although published studies indicate that its intracellular escape strategies play an important role in persistent cutaneous infections. This review provides current scientific knowledge about the intracellular life cycle of S. aureus in skin cells, which can be classified into professional and non-professional antigen-presenting cells, and its strategies to escape adaptive defense mechanisms. First, we discuss phenotypic switch of S. aureus, which affects intracellular routing and degradation. This review also evaluates potential intracellular escape mechanism of S. aureus to avoid intracellular degradation and antigen presentation, preventing an immune response. Furthermore, we discuss potential drug targets that can interfere with the intracellular life cycle of S. aureus. Taken together, this review aimed to increase scientific understanding about the intracellular life cycle of S. aureus into skin cells and its strategies to evade the host immune response, information that is crucial to reduce pathogenic invasion and life-threatening persistence of S. aureus in chronic cutaneous infections.
Indexed as
Identifiers
What Socratic 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 Socratic graph.