ArticleJournal of Korean medical science2006
Role of staphylococcal superantigen in atopic dermatitis: influence on keratinocytes.
Article in Journal of Korean medical science, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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.
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
11 citing papers in PubMed, 34 citations in OpenAlex.
- Microbiome and Postbiotics in Skin Health.Biomedicines · 2025Review
- Manipulating Microbiota to Treat Atopic Dermatitis: Functions and Therapies.Pathogens (Basel, Switzerland) · 2022Review
- Cutaneous dysbiosis may amplify barrier dysfunction in patients with atopic dermatitis.Frontiers in microbiology · 2022Article
- Hyperkeratinization and Proinflammatory Cytokine Expression in Meibomian Glands Induced by Staphylococcus aureus.Investigative ophthalmology & visual science · 2021Article
- The Keratinocyte as a Crucial Cell in the Predisposition, Onset, Progression, Therapy and Study of the Atopic Dermatitis.International journal of molecular sciences · 2021Review
- Phosphatidylinositol-specific phospholipase C enhances epidermal penetration by Staphylococcus aureus.Scientific reports · 2020Article
- Staphylococcus aureus Induces Increased Serine Protease Activity in Keratinocytes.The Journal of investigative dermatology · 2017Article
- The role of the skin microbiome in atopic dermatitis.Current allergy and asthma reports · 2015Review
- Potential Immunoinflammatory Role of Staphylococcal Enterotoxin A in Atopic Dermatitis: Immunohistopathological Analysis and in vitro Assay.Annals of dermatology · 2013Article
- Exogenous control of the expression of Group I CD1 molecules competent for presentation of microbial nonpeptide antigens to human T lymphocytes.Clinical & developmental immunology · 2011Review
- Role of Cutaneous Microbiome in Dermatology.Indian journal of dermatologyArticle
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Staphylococcus aureus may perform an crucial function in atopic dermatitis (AD), via the secretion of superantigens, including staphylococcal enterotoxins (SE) A or B, and toxic shock syndrome toxin-1 (TSST-1). Dysregulated cytokine production by keratinocytes (KCs) upon exposure to staphylococcal superantigens (SsAgs) may be principally involved in the pathophysiology of AD. We hypothesized that lesional KCs from AD may react differently to SsAgs compared to nonlesional skin or normal skin from nonatopics. We conducted a comparison of HLA-DR or CD1a expression in lesional skin as opposed to that in nonlesional or normal skin by immunohistochemistry (IHC). We also compared, using ELISA, the levels of IL-1alpha, IL-1beta, and TNF-alpha secreted by cultured KCs from lesional, nonlesional, and normal skin, after the addition of SEA, SEB and TSST-1. IHC revealed that both HLA-DR and CD1a expression increased significantly in the epidermis of lesional skin versus nonlesional or normal skin in quite a similar manner. IL-1alpha, IL-1beta, and TNF-alpha secretion was also significantly elevated in the cultured KCs from lesional skin after the addition of SsAgs. Our results indicated that KCs from lesional skin appear to react differently to SsAgs and increased proinflammatory cytokine production in response to SsAgs may contribute to the pathogenesis of AD.
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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.