Bacterial Pyocyanin Inducible Keratin 6A Accelerates Closure of Epithelial Defect under Conditions of Mitochondrial Dysfunction.
Journal
The Journal of investigative dermatology
ISSN: 1523-1747
Titre abrégé: J Invest Dermatol
Pays: United States
ID NLM: 0426720
Informations de publication
Date de publication:
10 2023
10 2023
Historique:
received:
10
09
2021
revised:
13
03
2023
accepted:
19
03
2023
pmc-release:
01
10
2024
medline:
25
9
2023
pubmed:
13
4
2023
entrez:
12
4
2023
Statut:
ppublish
Résumé
Repair of epithelial defect is complicated by infection and related metabolites. Pyocyanin (PYO) is one such metabolite that is secreted during Pseudomonas aeruginosa infection. Keratinocyte (KC) migration is required for the closure of skin epithelial defects. This work sought to understand PYO-KC interaction and its significance in tissue repair. Stable Isotope Labeling by Amino acids in Cell culture proteomics identified mitochondrial dysfunction as the top pathway responsive to PYO exposure in human KCs. Consistently, functional studies showed mitochondrial stress, depletion of reducing equivalents, and adenosine triphosphate. Strikingly, despite all stated earlier, PYO markedly accelerated KC migration. Investigation of underlying mechanisms revealed, to our knowledge, a previously unreported function of keratin 6A in KCs. Keratin 6A was PYO inducible and accelerated closure of epithelial defect. Acceleration of closure was associated with poor quality healing, including compromised expression of apical junction proteins. This work recognizes keratin 6A for its role in enhancing KC migration under conditions of threat posed by PYO. Qualitatively deficient junctional proteins under conditions of defensive acceleration of KC migration explain why an infected wound close with deficient skin barrier function as previously reported.
Identifiants
pubmed: 37044260
pii: S0022-202X(23)01964-4
doi: 10.1016/j.jid.2023.03.1671
pmc: PMC10529774
mid: NIHMS1922201
pii:
doi:
Substances chimiques
Pyocyanine
9OQM399341
Keratin-6
0
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
2052-2064.e5Subventions
Organisme : NIH HHS
ID : S10 OD018056
Pays : United States
Organisme : NINR NIH HHS
ID : R01 NR013898
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL131941
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK125835
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA270608
Pays : United States
Commentaires et corrections
Type : CommentIn
Informations de copyright
Copyright © 2023 The Authors. Published by Elsevier Inc. All rights reserved.
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