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Staphylococcus aureus causes aberrant epidermal lipid composition and skin barrier dysfunction.

Jihyun Kim1,2, Byung Eui Kim1,2, Evgeny Berdyshev3

  • 1Department of Pediatrics, National Jewish Health, Denver, Colorado, USA.

Allergy
|January 7, 2023
PubMed
Summary

Staphylococcus aureus colonization in atopic dermatitis disrupts skin lipids and barrier function by inhibiting fatty acid elongase enzymes, with methicillin-resistant S. aureus showing a more pronounced effect.

Keywords:
Staphylococcus aureusatopic dermatitisceramideselongaseskin barrier

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Area of Science:

  • Dermatology
  • Microbiology
  • Biochemistry

Background:

  • Staphylococcus aureus colonization is a known factor in atopic dermatitis (AD) pathogenesis.
  • The specific mechanisms by which S. aureus alters epidermal lipid composition and impairs skin barrier function in AD remain unclear.

Purpose of the Study:

  • To investigate the impact of S. aureus colonization on epidermal lipid profiles and skin barrier function in children with AD.
  • To elucidate the role of methicillin-sensitive S. aureus (MSSA) and methicillin-resistant S. aureus (MRSA) in inducing these changes.

Main Methods:

  • Lipidomic analysis of skin tape strips from children with AD and healthy controls.
  • Quantification of S. aureus (MSSA and MRSA) skin colonization levels.
  • In vitro studies using human keratinocytes and organotypic skin cultures to assess the effects of S. aureus.

Main Results:

  • MRSA-colonized AD skin exhibited altered lipid profiles, including increased ceramides, sphingomyelins, and lysophosphatidylcholines, with a reduction in very long-chain fatty acids (VLCFAs).
  • Increased transepidermal water loss (TEWL) was observed in MRSA-colonized AD skin.
  • S. aureus, particularly MRSA, inhibited fatty acid elongase (ELOVL3 and ELOVL4) expression in keratinocytes, mediated by inflammatory cytokines (IL-1β, TNF-α, IL-6, IL-33), leading to barrier dysfunction.

Conclusions:

  • S. aureus colonization is directly associated with aberrant skin lipid profiles and impaired barrier function in atopic dermatitis.
  • The observed effects are mediated by S. aureus-induced inhibition of ELOVL enzymes through inflammatory cytokines, with MRSA demonstrating a more significant impact than MSSA.