Mixed-species biofilm compromises wound healing by disrupting epidermal barrier function

In chronic wounds, biofilm infects host tissue for extended periods of time. This work establishes the first chronic preclinical model of wound biofilm infection aimed at addressing the long‐term host response. Although biofilm‐infected wounds did not show marked differences in wound closure, the re...

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Veröffentlicht in:The Journal of pathology 2014-08, Vol.233 (4), p.331-343
Hauptverfasser: Roy, Sashwati, Elgharably, Haytham, Sinha, Mithun, Ganesh, Kasturi, Chaney, Sarah, Mann, Ethan, Miller, Christina, Khanna, Savita, Bergdall, Valerie K, Powell, Heather M, Cook, Charles H, Gordillo, Gayle M, Wozniak, Daniel J, Sen, Chandan K
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container_end_page 343
container_issue 4
container_start_page 331
container_title The Journal of pathology
container_volume 233
creator Roy, Sashwati
Elgharably, Haytham
Sinha, Mithun
Ganesh, Kasturi
Chaney, Sarah
Mann, Ethan
Miller, Christina
Khanna, Savita
Bergdall, Valerie K
Powell, Heather M
Cook, Charles H
Gordillo, Gayle M
Wozniak, Daniel J
Sen, Chandan K
description In chronic wounds, biofilm infects host tissue for extended periods of time. This work establishes the first chronic preclinical model of wound biofilm infection aimed at addressing the long‐term host response. Although biofilm‐infected wounds did not show marked differences in wound closure, the repaired skin demonstrated compromised barrier function. This observation is clinically significant, because it leads to the notion that even if a biofilm infected wound is closed, as observed visually, it may be complicated by the presence of failed skin, which is likely to be infected and/or further complicated postclosure. Study of the underlying mechanisms recognized for the first time biofilm‐inducible miR‐146a and miR‐106b in the host skin wound‐edge tissue. These miRs silenced ZO‐1 and ZO‐2 to compromise tight junction function, resulting in leaky skin as measured by transepidermal water loss (TEWL). Intervention strategies aimed at inhibiting biofilm‐inducible miRNAs may be productive in restoring the barrier function of host skin. Copyright © 2014 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
doi_str_mv 10.1002/path.4360
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This work establishes the first chronic preclinical model of wound biofilm infection aimed at addressing the long‐term host response. Although biofilm‐infected wounds did not show marked differences in wound closure, the repaired skin demonstrated compromised barrier function. This observation is clinically significant, because it leads to the notion that even if a biofilm infected wound is closed, as observed visually, it may be complicated by the presence of failed skin, which is likely to be infected and/or further complicated postclosure. Study of the underlying mechanisms recognized for the first time biofilm‐inducible miR‐146a and miR‐106b in the host skin wound‐edge tissue. These miRs silenced ZO‐1 and ZO‐2 to compromise tight junction function, resulting in leaky skin as measured by transepidermal water loss (TEWL). Intervention strategies aimed at inhibiting biofilm‐inducible miRNAs may be productive in restoring the barrier function of host skin. Copyright © 2014 Pathological Society of Great Britain and Ireland. 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Pathol</addtitle><description>In chronic wounds, biofilm infects host tissue for extended periods of time. This work establishes the first chronic preclinical model of wound biofilm infection aimed at addressing the long‐term host response. Although biofilm‐infected wounds did not show marked differences in wound closure, the repaired skin demonstrated compromised barrier function. This observation is clinically significant, because it leads to the notion that even if a biofilm infected wound is closed, as observed visually, it may be complicated by the presence of failed skin, which is likely to be infected and/or further complicated postclosure. Study of the underlying mechanisms recognized for the first time biofilm‐inducible miR‐146a and miR‐106b in the host skin wound‐edge tissue. These miRs silenced ZO‐1 and ZO‐2 to compromise tight junction function, resulting in leaky skin as measured by transepidermal water loss (TEWL). Intervention strategies aimed at inhibiting biofilm‐inducible miRNAs may be productive in restoring the barrier function of host skin. Copyright © 2014 Pathological Society of Great Britain and Ireland. 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subjects Acinetobacter baumannii - physiology
Animals
Biofilms
Cell Membrane Permeability - physiology
Debridement
Epidermis - physiopathology
In Vitro Techniques
Male
Mice
Mice, Inbred C57BL
microRNA
MicroRNAs - metabolism
mixed-species biofilm
Models, Animal
porcine burn wounds
Pseudomonas aeruginosa - physiology
Skin - metabolism
Swine
transepidermal water loss (TEWL)
wound biofilm
Wound Healing - physiology
Zonula Occludens-1 Protein - metabolism
Zonula Occludens-2 Protein - metabolism
title Mixed-species biofilm compromises wound healing by disrupting epidermal barrier function
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