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Human Beta Defensin-2-mediated protection of human skin barrier in vitro; a mechanistic evaluation

ABSTRACT: I this project we performed global proteomic and secretomic analyses, following HBD2 stimulation, with or without V8-mediated damage, demonstrating minimal impact of the peptide alone on undamaged cells and showing that HBD2 did not induce expression of known antiproteases, but rather may function by modulating expression of extracellular matrix proteins.

INSTRUMENT(S): Q Exactive Plus

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Keratinocyte, Skin

DISEASE(S): Atopic Dermatitis

SUBMITTER: Jimi Wills

LAB HEAD: Donald J. Davidson

PROVIDER: PXD037844 | Pride | 2023-02-09

REPOSITORIES: Pride

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			Action	DRS
	cells02_hBD2-V8-1.raw	Raw
	cells03_TNFa-1.raw	Raw
	cells04_V8-1.raw	Raw
	cells05_WT-1.raw	Raw
	cells06_IL1B100-1.raw	Raw

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A mechanistic evaluation of human beta defensin 2 mediated protection of human skin barrier in vitro.

Project description:The human skin barrier, a biological imperative, is impaired in inflammatory skin diseases such as atopic dermatitis (AD). Staphylococcus aureus is associated with AD lesions and contributes to pathological inflammation and further barrier impairment. S. aureus secretes extracellular proteases, such as V8 (or 'SspA'), which cleave extracellular proteins to reduce skin barrier. Previous studies demonstrated that the host defence peptide human beta-defensin 2 (HBD2) prevented V8-mediated damage. Here, the mechanism of HBD2-mediated barrier protection in vitro is examined. Application of exogenous HBD2 provided protection against V8, irrespective of timeline of application or native peptide folding, raising the prospect of simple peptide analogues as therapeutics. HBD2 treatment, in context of V8-mediated damage, modulated the proteomic/secretomic profiles of HaCaT cells, altering levels of specific extracellular matrix proteins, potentially recovering V8 damage. However, HBD2 alone did not substantially modulate cellular proteomic/secretomics profiles in the absence of damage, suggesting possible therapeutic targeting of lesion damage sites only. HBD2 did not show any direct protease inhibition or induce expression of known antiproteases, did not alter keratinocyte migration or proliferation, or form protective nanonet structures. These data validate the barrier-protective properties of HBD2 in vitro and establish key protein datasets for further targeted mechanistic analyses.

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