Regulation of epidermal tight-junctions (TJ) during infection with exfoliative toxin-negative Staphylococcus strains
Open accessAbstract
Tight Junction (TJ) proteins have been shown to exert a barrier function within the skin. Here, we study the fate of TJ proteins during the challenge of the skin by bacterial colonization and infection. We investigated the influence of various exfoliative toxin-negative Staphylococcus strains on TJ, adherens junction (AJ), desmosomal proteins, and actin in a human keratinocyte infection culture and in a porcine skin infection model. We found that the pathogen Staphylococcus aureus downregulates TJ and subsequently AJ and desmosomal proteins, including atypical protein kinase C, an essential player in TJ formation, at the cell-cell borders of keratinocytes in a time and concentration dependent manner. Little changes in protein and RNA levels were seen, indicating redistribution of proteins. In cultured keratinocytes, a reduction of transepithelial resistance was observed. Staphylococcus epidermidis shows only minor effects. All strains induced enhanced expression of occludin and ZO-1 at the beginning of colonization/infection. Thus, we demonstrate that TJ are likely to be involved in skin infection of exfoliative toxin-negative S. aureus. As we did not find a change in actin, and as changes of TJ preceded alterations of AJs and desmosomes, we suggest that S. aureus targets TJ.
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The expression of subunit proteins such as claudins and occludins is reduced by exposure to allergens and staphylococcal strains, compromising barrier integrity in AD.
“The expression of subunit proteins such as claudins and occludins is reduced by exposure to allergens and staphylococcal strains, compromising barrier integrity in AD.”
From Update on the pathogenesis of atopic dermatitis. (2024) · cites this paper as [45]
Staphylococcus epidermidis inhibits colonization by pathogenic S. aureus and induces AMP expression, resulting in innate immune alertness; it may also enhance epidermal barrier function by increasing expression of tight-junction proteins occludin and ZO-1.
“For example, the natural cutaneous commensal, Staphylococcus epidermidis inhibits the colonization by the pathogenic S. aureus and induces the expression of AMPs, resulting in S. epidermidis-orchestrated innate immune alertness; additionally, it may enhance the epidermal barrier function stimulating the increased expression of the tight-junction proteins, occludin and ZO-1 [124,125].”
From Recreating Human Skin In Vitro: Should the Microbiota Be Taken into Account? (2024) · cites this paper as [125]
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Skin barrier defects in atopic dermatitis
Agrawal, R., & Woodfolk, J. A. (2014) · Current Allergy and Asthma Reports · doi:10.1007/s11882-014-0433-9 · Cited by 201 · see citing works
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Recreating Human Skin In Vitro: Should the Microbiota Be Taken into Account?
Galvan, A., Pellicciari, C., & Calderan, L. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms25021165 · Cited by 11 · see citing works
- Authors
- Ohnemus, U., Kohrmeyer, K., Houdek, P., Rohde, H., Wladykowski, E., Vidal, S., Horstkotte, M. A., Aepfelbacher, M., Kirschner, N., Behne, M. J., Moll, I., & Brandner, J. M.
- Affiliations
- University Medical Center Hamburg-Eppendorf (DE)
- Corresponding author
- Brandner, Johanna M.
- Venue
- Journal of Investigative Dermatology
- Publisher
- Elsevier BV
- Published
- 2008-04
- Volume
- 128
- Issue
- 4
- Pages
- 906-916
- ISSN
- 0022-202X (ISSN-L)
- OpenAlex
- W1981866488
- Cited by
- 124
- References
- 2
- Citations by year
- 2026: 5 · 2025: 9 · 2024: 7 · 2023: 7 · 2022: 10 · 2021: 8 · 2020: 9 · 2019: 6 · 2018: 5 · 2017: 4 · 2016: 6 · 2015: 5 · 2014: 10 · 2013: 8 · 2012: 6
- FWCI
- 3.36
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Journal of Investigative Dermatology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Infectious Diseases › Antimicrobial Resistance in Staphylococcus
- Health Sciences › Medicine › Dermatology › Dermatology and Skin Diseases
- Life Sciences › Neuroscience › Neurology › Barrier Structure and Function Studies
- Keywords
- tight junctions, Staphylococcus aureus, Staphylococcus epidermidis, skin infections, keratinocytes, adherens junctions, desmosomes, atypical protein kinase C, occludin, ZO-1, transepithelial electrical resistance, skin barrier, bacterial colonization, porcine skin model
- MeSH terms
- Actins, Animals, Desmosomes, Disease Models, Animal, Epidermis, Humans, Membrane Proteins, Phosphoproteins, Staphylococcal Infections, Staphylococcus aureus, Staphylococcus epidermidis, Tight Junctions, Adherens Junctions, Occludin, Zonula Occludens-1 Protein
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