AI Article Synopsis
- Staphylococcus aureus (SA) colonizes and harms skin in atopic dermatitis, while Staphylococcus epidermidis (SE) can reduce SA's harmful effects.
- Researchers created a model called a virtual skin site to explore how SA, SE, and the skin barrier interact in atopic dermatitis, leading to skin damage.
- The study found that stronger growth inhibition of SA by SE prevented skin damage, suggesting a combination treatment targeting both bacteria may restore healthier skin better than just killing SA alone.
Article Abstract
(SA) colonizes and can damage skin in atopic dermatitis lesions, despite being commonly found with (SE), a commensal that can inhibit SA's virulence and kill SA. In this study, we developed an model, termed a virtual skin site, describing the dynamic interplay between SA, SE, and the skin barrier in atopic dermatitis lesions to investigate the mechanisms driving skin damage by SA and SE. We generated 10 virtual skin sites by varying model parameters to represent different skin physiologies and bacterial properties. analysis revealed that virtual skin sites with no skin damage in the model were characterized by parameters representing stronger SA and SE growth attenuation than those with skin damage. This inspired an treatment strategy combining SA-killing with an enhanced SA-SE growth attenuation, which was found through simulations to recover many more damaged virtual skin sites to a non-damaged state, compared with SA-killing alone. This study demonstrates that modelling can help elucidate the key factors driving skin damage caused by SA-SE colonization in atopic dermatitis lesions and help propose strategies to control it, which we envision will contribute to the design of promising treatments for clinical studies.
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|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11101946 | PMC |
| http://dx.doi.org/10.1016/j.xjidi.2024.100269 | DOI Listing |
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