Keratinocyte and Fibroblast Wound Healing In Vitro Is Repressed by Non-Optimal Conditions but the Reparative Potential Can Be Improved by Water-Filtered Infrared A.

Cornelia Wiegand,Jörg Tittelbach,Uta-Christina Hipler,Peter Elsner

doi:10.3390/biomedicines9121802

Cornelia Wiegand, Jörg Tittelbach + Show 2 more

Open Access

https://doi.org/10.3390/biomedicines9121802

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Journal: Biomedicines	Publication Date: Nov 30, 2021
Citations: 16	License type: CC BY 4.0

Affiliation: Jena University Hospital

Abstract

It is a general goal to improve wound healing, especially of chronic wounds. As light therapy has gained increasing attention, the positive influence on healing progression of water-filtered infrared A (wIRA), a special form of thermal radiation, has been investigated and compared to the detrimental effects of UV-B irradiation on wound closure in vitro. Models of keratinocyte and fibroblast scratches help to elucidate effects on epithelial and dermal healing. This study further used the simulation of non-optimal settings such as S. aureus infection, chronic inflammation, and anti-inflammatory conditions to determine how these affect scratch wound progression and whether wIRA treatment can improve healing. Gene expression analysis for cytokines (IL1A, IL6, CXCL8), growth (TGFB1, PDGFC) and transcription factors (NFKB1, TP53), heat shock proteins (HSP90AA1, HSPA1A, HSPD1), keratinocyte desmogleins (DSG1, DSG3), and fibroblast collagen (COL1A1, COL3A1) was performed. Keratinocyte and fibroblast wound healing under non-optimal conditions was found to be distinctly reduced in vitro. wIRA treatment could counteract the inflammatory response in infected keratinocytes as well as under chronic inflammatory conditions by decreasing pro-inflammatory cytokine gene expression and improve wound healing. In contrast, in the anti-inflammatory setting, wIRA radiation could re-initiate the acute inflammatory response necessary after injury to stimulate the regenerative processes and advance scratch closure.

Highlights

Wound healing is a complex process in which different epidermal and dermal cell types as well as leukocytes are involved and is coordinated by cytokines and growth factors [1]
Gene expression analysis was performed for pro-inflammatory cytokines, growth factors, transcription factors, and stress response genes as well as desmogleins such as cell adhesion molecules and antimicrobial peptides for keratinocytes along with collagen 1 and 3 in the case of fibroblasts to investigate their profiles during wound healing
The influence was most pronounced for the infection with S. aureus, which damaged the cells to an extent that scratch wounds did not heal in vitro

Summary

Introduction

Wound healing is a complex process in which different epidermal and dermal cell types as well as leukocytes are involved and is coordinated by cytokines and growth factors [1]. Prolonged inflammation delays wound closure by preventing the transition from degrading to proliferative processes [4]. Chronic wounds represent a major challenge in hospitals and health care settings. These wounds may remain non-healing due to a microbial infection [5,6] and continuous inflammatory conditions [7]. Anti-inflammatory conditions have been reported to affect wound healing processes [8,9,10]

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