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• W2013174909 abstract "human skin equivalent Full thickness burns, in contrast to cold injury wounds, heal with significant (hypertrophic) scarring and contraction (Martin, 1997Martin P. Wound healing – aiming for perfect skin regeneration.Science. 1997; 276: 75-81Crossref PubMed Scopus (3430) Google Scholar; Camp et al., 2003Camp D.F. Ateaque A. Dickson W.A. Cryogenic burns from aerosol sprays: a report of two cases and review of the literature.Br J Plast Surg. 2003; 56: 815-817Abstract Full Text Full Text PDF PubMed Scopus (17) Google Scholar). Optimal scar formation is dependent on early factors regulating wound closure and inflammation. Upon wounding, keratinocytes immediately adjacent to the wound edge proliferate and migrate into the wound gap in order to close the wound (Saarialho-Kere et al., 1994Saarialho-Kere U.K. Pentland A.P. Birkedal-Hansen H. Parks W.C. Welgus H.G. Distinct populations of basal keratinocytes express stromelysin-1 and stromelysin-2 in chronic wounds.J Clin Invest. 1994; 94: 79-88Crossref PubMed Scopus (197) Google Scholar, Saarialho-Kere et al., 1995Saarialho-Kere U.K. Vaalamo M. Airola K. Niemi K.M. Oikarinen A.I. Parks W.C. Interstitial collagenase is expressed by keratinocytes that are actively involved in reepithelialization in blistering skin disease.J Invest Dermatol. 1995; 104: 982-988Crossref PubMed Scopus (61) Google Scholar). This process of re-epithelialization has been shown to involve interactions between keratinocytes and fibroblasts. The inflammatory response of wound healing occurs parallel to re-epithelialization. It involves the secretion of inflammatory mediators (chemokines) which regulate infiltration of neutrophils macrophages and lymphocytes into the wound bed (Engelhardt et al., 1998Engelhardt E. Toksoy A. Goebeler M. Debus S. Brocker E.B. Gillitzer R. Chemokines IL-8, GROalpha, MCP-1, IP-10, and Mig are sequentially and differentially expressed during phase-specific infiltration of leukocyte subsets in human wound healing.Am J Pathol. 1998; 153: 1849-1860Abstract Full Text Full Text PDF PubMed Scopus (328) Google Scholar). These inflammatory mediators also stimulate angiogenesis, mitogenesis, and dermal remodeling (Martin, 1997Martin P. Wound healing – aiming for perfect skin regeneration.Science. 1997; 276: 75-81Crossref PubMed Scopus (3430) Google Scholar; Gillitzer and Goebeler, 2001Gillitzer R. Goebeler M. Chemokines in cutaneous wound healing.J Leukoc Biol. 2001; 69: 513-521PubMed Google Scholar). In this study, we established in how far human skin equivalents (HSEs) (human reconstructed epidermis on fibroblast-populated rat-collagen gels) (Bell et al., 1981Bell E. Ehrlich H.P. Buttle D.J. Nakatsuji T. Living tissue formed in vitro and accepted as skin-equivalent tissue of full thickness.Science. 1981; 211: 1052-1054Crossref PubMed Scopus (811) Google Scholar; Spiekstra et al., 2005Spiekstra S.W. Toebak M.J. Sampat-Sardjoepersad S. van Beek P.J. Boorsma D.M. Stoof T.J. et al.Induction of cytokine (interleukin-1 alpha and tumor necrosis factor-alpha) and chemokine (CCL20, CCL27, and CXCL8) alarm signals after allergen and irritant exposure.Exp Dermatol. 2005; 14: 109-116Crossref PubMed Scopus (82) Google Scholar) can be used to reproduce histological observations associated with burn and cold injury in vivo. We determined novel similarities and differences involved in the closure of these two very different types of wound in the fully defined, in vitro, HSEs wound-healing model. As immune infiltrating cells and other skin residential cells (e.g., Langerhans Cells, macrophages, monocytes, mast cells, and endothelial cells) are not present in the HSEs, we are able to report events entirely due to keratinocyte–fibroblast interactions. The unwounded region of HSEs consists of fully reconstructed epidermis containing a compact basal layer, spinous layer, granular layer, and stratum corneum on a fibroblast-populated collagen gel. Burn injury resulted in destruction of the epidermis and death of fibroblasts (seen by elongated fibroblasts become rounded and necrotic) (Figure 1a). After burning, wound contraction occurred (width of device used to inflict wound=2.0 mm; width of wound after 24 hours=1 mm±0.21, n=12). These findings correlate to those obtained after burning ex vivo skin (data not shown) and also to in vivo observations after burning (Li et al., 1980Li A.K. Ehrlich H.P. Trelstad R.L. Koroly M.J. Schattenkerk M.E. Malt R.A. Differences in healing of skin wounds caused by burn and freeze injuries.Ann Surg. 1980; 191: 244-248Crossref PubMed Scopus (74) Google Scholar; Ehrlich and Hembry, 1984Ehrlich H.P. Hembry R.M. A comparative study of fibroblasts in healing freeze and burn injuries in rats.Am J Pathol. 1984; 117: 218-224PubMed Google Scholar). In contrast to burns, extreme cold injury did not result in destruction of the epidermis of HSEs (Figure 1b). Cells showed characteristics of necrosis (not apoptosis) with rounded nuclei in both the frozen areas of the epidermis and dermis. Notably, a clear separation of the epidermis from the dermis at the basement membrane zone (blistering) was observed in HSEs only in the area of the cold injury. No wound contraction occurred after 24 hours. On the contrary the wound margins were 2.56 mm±0.77, n=12 which is slightly wider than the width of the device used to inflict wounds (2 mm). These findings correlate to those after inflicting cold injury to ex vivo skin (data not shown) and also to in vivo observations after extreme cold injury (Shepherd and Dawber, 1984Shepherd J.P. Dawber R.P. Wound healing and scarring after cryosurgery.Cryobiology. 1984; 21: 157-169Crossref PubMed Scopus (83) Google Scholar; Matook et al., 1994Matook G.M. Sasken H. Akelman E. Propane thermal injuries: case report and review of the literature.J Trauma. 1994; 37: 318-321Crossref PubMed Scopus (10) Google Scholar). After both burn and cold injury, regenerating epidermis formed underneath the dead epidermal tissue (Figure 1a and b). Re-epithelialization occurred from both sides of the wound margins until the fronts met and closed the wound. At 2 days after wounding, the intermediate zone showed a fully differentiated morphology including the presence of stratum corneum. Fibroblast migration lagged behind keratinocyte migration and was not observed until 7 days after injury. The rate of re-epithelialization was significantly slower after introduction of burns compared to cold injury. At 2 days after wounding, the burn wound front had migrated 450±30 μm compared to the cold injury wound front which had migrated 950±60 μm (P<0.01). The morphology of the migrating fronts of the two types of wounds also showed different morphological characteristics. In burns, the migrating front was rounded and multi-layered (Figure 1a, inset). Many proliferating keratinocytes were present in the basal layer and also suprabasal layers indicating that the migrating front was hyper-proliferative (Figure 1d) compared to unwounded areas of the HSEs (Figure 1c). The outermost region was clearly detached from the collagen gel. In contrast, after cold injury only sporadic proliferating keratinocytes could be detected and the migrating front was pointed with a single keratinocyte at the outermost point (Figure 1b, e, and f). Also in contrast to burns, the outermost region was clearly attached to the collagen gel. These observations led us to determine whether the expression of basement membrane proteins was affected upon wounding. After burning, basement membrane proteins (collagen type IV, collagen type VII, heparan sulfate proteoglycan, laminin) could no longer be detected by immuno-histochemical analysis indicating that these components of the basement membrane had been destroyed in both excised skin (data not shown) and HSEs (Figure 1g and h shows representative staining for collagen type IV and laminin 5, respectively). In HSEs, just behind the outermost migrating front and in the intermediary region, the basement membrane proteins could again be detected indicating that they have been resynthesized by keratinocyte–fibroblast interactions (El Ghalbzouri et al., 2005El Ghalbzouri A. Jonkman M.F. Dijkman R. Ponec M. Basement membrane reconstruction in human skin equivalents is regulated by fibroblasts and/or exogenously activated keratinocytes.J Invest Dermatol. 2005; 124: 79-86Crossref PubMed Scopus (86) Google Scholar). In contrast to burning, after cold injury – all four basement membrane proteins could still be detected (Figure 1i and j). Retainment of the basement membrane after freezing is in agreement to results published by Langdon et al., 1988Langdon R.C. Cuono C.B. Birchall N. Madri J.A. Kuklinska E. McGuire J. et al.Reconstitution of structure and cell function in human skin grafts derived from cryopreserved allogeneic dermis and autologous cultured keratinocytes.J Invest Dermatol. 1988; 91: 478-485Abstract Full Text PDF PubMed Google Scholar. Our results indicate that after burning, in contrast to after cold injury, the basement membrane is damaged and has to be re-synthesized in order to permit re-epithelialization. In vivo, this may contribute to poor scar quality. Next we determined whether differences also occurred after burn and cold injury with regards to the secretion of inflammatory mediators which have already been implicated to play a role in (acute surgical) wound healing and epidermal damage in vivo (Gillitzer and Goebeler, 2001Gillitzer R. Goebeler M. Chemokines in cutaneous wound healing.J Leukoc Biol. 2001; 69: 513-521PubMed Google Scholar; Schmuth et al., 2002Schmuth M. Neyer S. Rainer C. Grassegger A. Fritsch P. Romani N. et al.Expression of the C-C chemokine MIP-3 alpha/CCL20 in human epidermis with impaired permeability barrier function.Exp Dermatol. 2002; 11: 135-142Crossref PubMed Scopus (86) Google Scholar). CCL5/RANTES, CCL20/MIP3α, CXCL1/GRO-α, CXCL8/IL-8 secretion was therefore investigated during closure of burn and cold injury wounds (Figure 2). An increase in secretion of all four inflammatory mediators was observed already within 24 hours after wounding. CCL20/MIP3α and CXCL8/IL-8 secretion declined when the wound closed (after 3 days) whereas CXCL1/GRO-α and CCL5/RANTES secretion remained high after wound closure. In our model, the secretion of all four inflammatory mediators in response to cellular damage was similar for both types of wound. It should not be forgotten however that we investigate only keratinocyte and fibroblast responses to wounding. These cells are at the first line of assault/tissue damage and give signals to the immune system thus initiating the immune response. Differences in the immune response/chemokine secretion may occur in the presence of other skin residential cells (Langerhans cells, macrophages, monocytes, mast cells, and endothelial cells) and once infiltrating cells and platelets have entered the damaged region and responded to the extent of tissue damage (this is currently under investigation). In vivo, major tissue repair is required after burn injury which results in more contraction and scar formation in contrast to cold injury (Li et al., 1980Li A.K. Ehrlich H.P. Trelstad R.L. Koroly M.J. Schattenkerk M.E. Malt R.A. Differences in healing of skin wounds caused by burn and freeze injuries.Ann Surg. 1980; 191: 244-248Crossref PubMed Scopus (74) Google Scholar; Ehrlich and Hembry, 1984Ehrlich H.P. Hembry R.M. A comparative study of fibroblasts in healing freeze and burn injuries in rats.Am J Pathol. 1984; 117: 218-224PubMed Google Scholar). In conclusion, while important morphological differences were observed between the two types of wound, no differences were observed in the profiles of secreted chemokines. Future studies are underway to extensively characterize the model with respect to dermal matrix damage/regeneration, re-epithelialization, and inflammatory mediators and also to incorporate other skin residential cells and infiltrating cells into the model. The in vitro wound-healing model described in this study can be used in the future to investigate early differences between healing after burn and cold injury and may provide a pre-clinical means to investigate novel therapeutics designed for optimal wound healing in a fully defined in vitro setting before progressing to animal or clinical studies. The VU University Medical Center has approved the experiments described in this letter. The authors state no conflict of interest. This research was financed by Euro Skin Bank, Beverwijk, The Netherlands." @default.
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• W2013174909 title "Comparison of Wound Closure after Burn and Cold Injury in Human Skin Equivalents" @default.
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