ArticleScientific reports2026
Advancing human skin models by integrating skin microbes for next-generation research.
Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Selective Modulation ofClinical, cosmetic and investigational dermatology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The skin barrier comprises interdependent physical, chemical, immunological, and microbial components, of which the latter is constituted by a community of microbes residing on the skin surface that restricts the expansion of opportunistic pathogens, modulates keratinocyte signaling pathways, and fosters immune tolerance. However, molecular and cellular dynamics of host-microbe interactions remain incompletely characterized, partly due to the limited availability of physiologically relevant and robust preclinical models. We aimed to establish 3D human skin equivalents (HSEs) in co-culture with representative skin commensals to investigate host responses across an in vitro cohort of six biological replicates. Well-characterized HSEs were inoculated with Staphylococcus aureus, Staphylococcus epidermidis, and Cutibacterium acnes. A 48-hour co-culture period enabled microbial expansion, during which S. aureus exhibited the most substantial outgrowth, and strain-dependent variability was observed for S. epidermidis. Assessment of epidermal morphogenesis revealed that S. aureus exerted largest structural impact, whereas C. acnes promoted keratinocyte proliferation. Furthermore, S. aureus elicited a pro-inflammatory response, characterized by elevated secretion of IL-8 and CXCL1. In conclusion, we developed a reproducible experimental framework dissecting host-microbe interactions in HSEs to demonstrate that S. aureus induced substantial alterations in epidermal architecture and inflammatory signaling, underscoring its pathogenic potential in cutaneous environments.
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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.