Aberrant recruitment of leukocytes defines poor wound healing in patients with recessive dystrophic epidermolysis bullosa.
Adolescent
Adult
Aged
Child
Child, Preschool
Cross-Sectional Studies
Epidermolysis Bullosa Dystrophica
/ complications
Female
Humans
Infant
Leukocytes
/ immunology
Male
Middle Aged
Receptors, CCR2
/ metabolism
Receptors, Interleukin-8B
/ metabolism
Skin
/ cytology
Wound Healing
/ immunology
Young Adult
Chronic wounds
Infiltrate
Leukocytic
Matrix-remodeling enzymes
RDEB
Vascularization
Wound healing
Journal
Journal of dermatological science
ISSN: 1873-569X
Titre abrégé: J Dermatol Sci
Pays: Netherlands
ID NLM: 9011485
Informations de publication
Date de publication:
Dec 2020
Dec 2020
Historique:
received:
21
08
2020
revised:
06
10
2020
accepted:
12
10
2020
pubmed:
5
11
2020
medline:
22
6
2021
entrez:
4
11
2020
Statut:
ppublish
Résumé
Poorly healing wounds are one of the major complications in patients suffering from recessive dystrophic epidermolysis bullosa (RDEB). At present, there are no effective means to analyze changes in cellular and molecular networks occurring during RDEB wound progression to predict wound outcome and design betted wound management approaches. To better define mechanisms influencing RDEB wound progression by evaluating changes in molecular and cellular networks. We developed a non-invasive approach for sampling and analysis of wound-associated constituents using wound-covering bandages. Cellular and molecular components from seventy-six samples collected from early, established and chronic RDEB wounds were evaluated by FACS-based immuno-phenotyping and ELISA. Our cross-sectional analysis determined that progression of RDEB wounds to chronic state is associated with the accumulation (up to 90 %) of CD16 Our data demonstrated that wound-covering bandages are useful for a non-invasive sampling and analysis of wound-associated constituents and that transition to poorly healing wounds in RDEB patients as associated with distinct changes in leukocytic infiltrates, matrix-remodeling enzymes and pro-angiogenic factors at wound sites.
Sections du résumé
BACKGROUND
BACKGROUND
Poorly healing wounds are one of the major complications in patients suffering from recessive dystrophic epidermolysis bullosa (RDEB). At present, there are no effective means to analyze changes in cellular and molecular networks occurring during RDEB wound progression to predict wound outcome and design betted wound management approaches.
OBJECTIVES
OBJECTIVE
To better define mechanisms influencing RDEB wound progression by evaluating changes in molecular and cellular networks.
METHODS
METHODS
We developed a non-invasive approach for sampling and analysis of wound-associated constituents using wound-covering bandages. Cellular and molecular components from seventy-six samples collected from early, established and chronic RDEB wounds were evaluated by FACS-based immuno-phenotyping and ELISA.
RESULTS
RESULTS
Our cross-sectional analysis determined that progression of RDEB wounds to chronic state is associated with the accumulation (up to 90 %) of CD16
CONCLUSIONS
CONCLUSIONS
Our data demonstrated that wound-covering bandages are useful for a non-invasive sampling and analysis of wound-associated constituents and that transition to poorly healing wounds in RDEB patients as associated with distinct changes in leukocytic infiltrates, matrix-remodeling enzymes and pro-angiogenic factors at wound sites.
Identifiants
pubmed: 33143962
pii: S0923-1811(20)30327-3
doi: 10.1016/j.jdermsci.2020.10.009
pii:
doi:
Substances chimiques
CCR2 protein, human
0
CXCR2 protein, human
0
Receptors, CCR2
0
Receptors, Interleukin-8B
0
Types de publication
Journal Article
Observational Study
Langues
eng
Sous-ensembles de citation
IM
Pagination
209-216Subventions
Organisme : NIAMS NIH HHS
ID : R01 AR064286
Pays : United States
Informations de copyright
Copyright © 2020 The Author(s). Published by Elsevier B.V. All rights reserved.
Déclaration de conflit d'intérêts
Declaration of Competing Interest The authors have no conflict of interest to declare.