Skin Epidermal Cells Research Articles

Weak Ultraviolet B Enhances the Mislocalization of Claudin-1 Mediated by Nitric Oxide and Peroxynitrite Production in Human Keratinocyte-Derived HaCaT Cells

A tight junction (TJ) makes a physical barrier in the epidermal cells of skin. Ultraviolet (UV) light may disrupt the TJ barrier, but the mechanism has not been well clarified. Weak UVB (5 mJ/cm2) caused mislocalization of claudin-1 (CLDN1), a component of the TJ strand, and disruption of TJ barrier in human keratinocyte-derived HaCaT cells. The UVB-induced mislocalization of CLDN1 was inhibited by monodansylcadaverine (MDC), a clathrin-dependent endocytosis inhibitor, suggesting that UVB enhances the internalization of CLDN1. Transepidermal electrical resistance and paracellular flux of lucifer yellow, a fluorescent hydrophilic marker, were rescued by MDC. UVB changed neither the total nor phosphorylation levels of CLDN1, but it increased both mono-ubiquitination and tyrosine nitration levels of CLDN1. Fluorescence measurements revealed that UVB increased intracellular free Ca2+, nitric oxide (NO), and peroxynitrite contents, which were inhibited by Opsin2 (OPN2) siRNA, suggesting that OPN2 functions as a UVB sensor. The effects of UVB were inhibited by an antagonist of transient receptor potential type vanilloid 1 (TRPV1) and Ca2+ chelator. Both NO donor and peroxynitrite donor induced the mislocalization of CLDN1 and disruption of TJ barrier, which were rescued by a NO synthase (NOS) inhibitor and a peroxynitrite scavenger. Weak UVB irradiation induced the disruption of TJ barrier mediated by mislocalization of CLDN1 in HaCaT cells. The OPN2/TRPV1/NOS signaling pathway may be a novel target for preventing destruction of the TJ barrier by UVB irradiation.

Investigation of Cytotoxicity Apoptotic and Inflammatory Responses of Biosynthesized Zinc Oxide Nanoparticles from Ocimum sanctum Linn in Human Skin Keratinocyte (Hacat) and Human Lung Epithelial (A549) Cells.

Pristine and engineered metal nanoparticles are widely applied in various fields of industry, and as consequences, they are useful as well as harmful to human health and environment. This study aimed at synthesizing the green zinc oxide nanoparticles (ZnNPs) using the leaf extract of Ocimum sanctum Linn and assessing its toxicity on human skin epidermal (HaCaT) and human lung epithelial (A549) cells. The synthesized green ZnNPs (gZnNPs) were characterized by using dynamic light scattering (DLS) and a high-resolution transmission electron microscope. The average size of gZnNPs obtained was 62 nm with a spherical shape. The effects of gZnNPs on the viability of HaCaT and A549 cells were investigated using tetrazolium salt (MTT) for 24 h. We have seen more reduction of cell viability of A549 cells in comparison to HaCaT cells. The induction of intracellular reactive oxygen species (ROS) was measured using DCFDA assay and showed a slightly high intensity of green fluorescence in A549 than HaCaT cells. The different oxidative stress biomarkers such as ROS generation and lipid peroxide were increased, and GSH was decreased in a dose-dependent manner. The apoptotic and necrotic effect of gZnNPs in both cells was carried out using Annexin-V-FITC and propidium iodide staining. More apoptotic and necrotic cells were found at a higher concentration of gZnNPs exposure. Also, we determined the effect of gZnNPs at the molecular level by evaluating the apoptotic and inflammatory markers, in which gZnNPs downregulated Bcl2 and upregulated Bax, caspase-3, and TNF-α in HaCaT and A549 cells. Ultimately, gZnNPs exerted toxicity and apoptosis in HaCaT and A549 cells.

Antibody-Based Targeted Interventions for the Diagnosis and Treatment of Skin Cancers.

Cutaneous malignancies most commonly arise from skin epidermal cells. These cancers may rapidly progress from benign to a metastatic phase. Surgical resection represents the gold standard therapeutic treatment of non-metastatic skin cancer while chemo- and/or radiotherapy are often used against metastatic tumors. However, these therapeutic treatments are limited by the development of resistance and toxic side effects, resulting from the passive accumulation of cytotoxic drugs within healthy cells. This review aims to elucidate how the use of monoclonal Antibodies (mAbs) targeting specific Tumor Associated Antigens (TAAs) is paving the way to improved treatment. These mAbs are used as therapeutic or diagnostic carriers that can specifically deliver cytotoxic molecules, fluorophores or radiolabels to cancer cells that overexpress specific target antigens. mAbs raised against TAAs are widely in use for e.g. differential diagnosis, prognosis and therapy of skin cancers. Antibody-Drug Conjugates (ADCs) particularly show remarkable potential. The safest ADCs reported to date use non-toxic photo-activatable Photosensitizers (PSs), allowing targeted Photodynamic Therapy (PDT) resulting in targeted delivery of PS into cancer cells and selective killing after light activation without harming the normal cell population. The use of near-infrared-emitting PSs enables both diagnostic and therapeutic applications upon light activation at the specific wavelengths. Antibody-based approaches are presenting an array of opportunities to complement and improve current methods employed for skin cancer diagnosis and treatment.

Expression of Laminin γ2 Proteolytic Fragments in Murine Skin Following Exposure to Sulfur Mustard.

Laminin-332 is a basement membrane protein composed of three genetically distinct polypeptide chains that actively promote both skin epidermal cell adhesion and migration. Proteolytic fragments of the laminin γ2 chain stimulate migration and scattering of keratinocytes and cancer cells. Sulfur mustard (SM) is a bifunctional alkylating agent that induces separation of basal keratinocytes from the dermal-epidermal junction and invokes a strong inflammatory response leading to delayed wound repair. In the present studies, the role of laminin γ2 in SM-induced skin injury and wound repair was investigated using the mouse ear vesicant model. We found that laminin γ2 chain mRNA was preferentially upregulated in mouse ear skin exposed to SM. In situ hybridization confirmed overexpression of laminin γ2 transcript. Western blot analysis showed increased protein expression of the full-length proform of laminin γ2 and smaller processed fragments of laminin γ2 in skin exposed to SM. Dual immunofluorescence labeling indicated that laminin γ2 fragments are prevalent in suprabasal keratinocytes behind the leading edge in areas of hyperplasia in injured skin. In addition, co-expression of laminin γ2 and the senescent marker, p16-INK4a was found to overlap with the hyperplastic migratory epithelial sheet. This observation is similar to hypermotile keratinocytes reported in invasive carcinoma cells. Overall, our studies indicate that laminin γ2 is preferentially expressed in skin post SM exposure and that protein expression appears to become progressively more fragmented. The laminin γ2 fragments may play a role in regulating SM-induced skin wound repair. Anat Rec, 2020. © 2020 American Association for Anatomy.

Impact of intercellular crosstalk between epidermal keratinocytes and dermal fibroblasts on skin homeostasis

Dermal fibroblasts seem critical for epidermal maturation and differentiation and recent work demonstrated that diseased fibroblasts may drive pathophysiological processes. Nevertheless, still very little is known about the actual crosstalk between epidermal keratinocytes and dermal fibroblasts and the impact of dermal fibroblasts on epidermal maturation and differentiation. Aiming for a more fundamental understanding of the impact of the cellular crosstalk between keratinocytes and fibroblasts on the skin homeostasis, we generated full-thickness skin equivalents with and without fibroblasts and subsequently analysed them for the expression of skin differentiation markers, their barrier function, skin lipid content and epidermal cell signalling. Skin equivalents without fibroblasts consistently showed an impaired differentiation and dysregulated expression of skin barrier and tight junction proteins, increased skin permeability, and a decreased skin lipid/protein ratio. Most interestingly, impaired Ras/Raf/ERK/MEK signalling was evident in skin equivalents without fibroblasts.Our data clearly indicate that the epidermal-dermal crosstalk between keratinocytes and fibroblasts is critical for adequate skin differentiation and that fibroblasts orchestrate epidermal differentiation processes.

Bucillamine Inhibits UVB-Induced MAPK Activation and Apoptosis in Human HaCaT Keratinocytes and SKH-1 Hairless Mouse Skin.

Ultraviolet B (UVB) radiation is known as a culprit in skin carcinogenesis. We have previously reported that bucillamine (N-[2-mercapto-2-methylpropionyl]-L-cysteine), a cysteine derivative with antioxidant and anti-inflammatory capacity, protects against UVB-induced p53 activation and inflammatory responses in mouse skin. Since MAPK signaling pathways regulate p53 expression and activation, here we determined bucillamine effect on UVB-mediated MAPK activation in vitro using human skin keratinocyte cell line HaCaT and in vivo using SKH-1 hairless mouse skin. A single low dose of UVB (30mJcm-2 ) resulted in increased JNK/MAPK phosphorylation and caspase-3 cleavage in HaCaT cells. However, JNK activation and casaspe-3 cleavage were inhibited by pretreatment of HaCaT cells with physiological doses of bucillamine (25 and 100µm). Consistent with these results, bucillamine pretreatment in mice (20mgkg-1 ) inhibited JNK/MAPK and ERK/MAPK activation in skin epidermal cells at 6-12 and 24h, respectively, after UVB exposure. Moreover, bucillamine attenuated UVB-induced Ki-67-positive cells and cleaved caspase-3-positive cells in mouse skin. These findings demonstrate that bucillamine inhibits UVB-induced MAPK signaling, cell proliferation and apoptosis. Together with our previous report, we provide evidence that bucillamine has a photoprotective effect against UV exposure.

Enhanced DNA-repair capacity and resistance to chemically induced carcinogenesis upon deletion of the phosphatase regulator NIPP1

Nuclear Inhibitor of PP1 (NIPP1) is a conserved regulatory subunit of protein phosphatase PP1. The selective deletion of NIPP1 in mouse liver parenchymal cells or skin epidermal cells culminates in a late-onset hyperproliferation of a subset of resident progenitor cells. Although a hyperplastic phenotype is usually tumor promoting, we show here that the absence of NIPP1 conferred a strong resistance to chemically induced hepatocellular or skin carcinoma. The ablation of NIPP1 did not affect the metabolism of the administered mutagens (diethylnitrosamine or 7,12-dimethylbenz[a]anthracene), but reduced the conversion of mutagen-induced covalent DNA modifications into cancer-initiating mutations. This reduced sensitivity to mutagens correlated with an enhanced DNA-damage response and an augmented expression of rate-limiting DNA-repair proteins (MGMT in liver, XPD and XPG in skin), hinting at an increased DNA-repair capacity. Our data identify NIPP1 as a repressor of DNA repair and as a promising target for novel cancer prevention and treatment therapies.

Transient receptor potential vanilloid 4 modulates ion balance through the isotocin pathway in zebrafish (Danio rerio).

Isotocin controls ion regulation through modulating the functions of ionocytes (also called mitochondria-rich cells or chloride cells). However, little is known about the upstream molecule of the isotocin system. Herein, we identify transient receptor potential vanilloid 4 (TRPV4), which regulates the mRNA and protein expressions of isotocin and affects ion regulation through the isotocin pathway. Double immunohistochemical results showed that TRPV4 is expressed in isotocinergic neurons in the hypothalamus of the adult zebrafish brain. To further elucidate the roles of TRPV4, we manipulated TRPV4 protein expression and evaluated its ionoregulatory functions in zebrafish embryos. TRPV4 gene knockdown with morpholino oligonucleotides decreased ionic contents (Na+, Cl-, and Ca2+) of whole larvae and the H+-secreting function of larval skin of zebrafish. mRNA expressions of ionocyte-related transporters, including H+-ATPase, the epithelial Ca2+ channel, and the Na+-Cl- cotransporter, were also suppressed in trpv4 morphants. Numbers of ionocytes (H+-ATPase-rich cells and Na+-K+-ATPase-rich cells) and epidermal stem cells in zebrafish larval skin also decreased after trpv4 knockdown. Our results showed that TRPV4 modulates ion balance through the isotocin pathway.

Expression of Concern: “Cadmium Induces Intracellular Ca2+- and H2O2-Dependent Apoptosis through JNK- and p53-Mediated Pathways in Skin Epidermal Cell line”

Expression of Concern: “Cadmium Induces Intracellular Ca2+- and H2O2-Dependent Apoptosis through JNK- and p53-Mediated Pathways in Skin Epidermal Cell line”

WIF1 Suppresses the Generation of Suprabasal Cells in Acanthotic Skin and Growth of Basal Cell Carcinomas upon Forced Overexpression

We analyzed the role of WIF1 in normal and acanthotic epidermis of 12-O-tetradecanoylphorbol-13-acetate (TPA) or all-trans-retinoic acid (ATRA)-treated and basal cell carcinoma (BCC)-bearing mice. WIF1 protein is located in the follicular infundibulum and interfollicular epidermis (IFE) in murine back skin. Within the hyperplastic epidermis of TPA- or ATRA-treated or BCC-bearing murine skin, WIF1 and Keratin 10 overlap in Ki67⁻ suprabasal layers, while basal epidermal layers expressing Ki67, and BCCs expressing Wif1 mRNA, are free of WIF1 protein. This is similar in human skin, with the exception that WIF1 protein is found in single Ki67⁻ basal epidermal cells in normal skin and additionally in Ki67+ cells in acanthotic skin. Wif1-deficiency enhances acanthosis of the murine BCC-associated epidermis, which is accompanied by an increase of Ki67+ and of Sca-1+ basal cells. WIF1 overexpression in allografted BCC-derived keratinocytes prevents growth and keratinization, involving enhanced phosphorylation of protein kinase C and extracellular signal-regulated kinase 1 and arguably factors secreted by the invivo environment. In summary, WIF1 protein marks suprabasal layers in the normal IFE. It is also present in the epidermis overlaying BCCs where it diminishes proliferation of basal cells and production of differentiating suprabasal cells. In addition, WIF1 can prevent proliferation and keratinization of BCC-related keratinocytes.

Immunological Memory of Psoriatic Lesions.

The natural course of psoriasis is the appearance of new lesions in the place of previous ones, which disappeared after a successful therapy. Recent studies of psoriasis etiopathogenesis showed that after psoriatic plaques have disappeared, in healthy skin we can still find a trace of inflammation in the form of tissue resident memory cells (TRM). They are originally responsible for protection against viral and bacterial infections in non-lymphatic tissues. In psoriatic inflammation, they are characterized by heterogeneity depending on their origin. CD8+ T cells TRM are abundantly present in psoriatic epidermis, while CD4+ TRM preferentially populate the dermis. In psoriasis, epidermal CD8+ TRM cells express CLA, CCR6, CD103 and IL-23R antigen and produce IL-17A during ex vivo stimulation. However, CD4+ CD103+ TRM can also colonize the epidermis and produce IL-22 during stimulation. Besides T cells, Th22 and epidermal DCs proved that epidermal cells in healed skin were still present and functioning after several years of disease remission. It explains the clinical phenomenon of the tendency of psoriatic lesions to relapse in the same location and it allows to develop new therapeutic strategies in the future.

AQP5 regulates the proliferation and differentiation of epidermal stem cells in skin aging.

The epidermis, the outermost layer of the skin, is the first barrier that comes into contact with the external environment. It plays an important role in resisting the invasion of harmful substances and microbial infections. The skin changes with age and external environmental factors. This study aimed to investigate epidermal stem cells during the process of aging. This study enrolled 9 volunteers with benign pigmented nevus for clinical dermatologic surgery. The phenotypes associated with skin aging changes such as skin wrinkles and elasticity of the unexposed/healthy parts near benign pigmented skin were measured, and epidermal stem cells from this region were isolated for transcriptome sequencing. The results showed that epidermal stem cells could be obtained by magnetic activated cell sorting (MACS) with high purity. Results of the transcriptome sequencing revealed that aquaporin (AQP)5 significantly decreased in the epidermal stem cells with age, and further functional experiments revealed that AQP5 could promote the proliferation and dedifferentiation of HaCaT, but did not influence cell apoptosis. In summary, AQP5 regulated the proliferation and differentiation of epidermal stem cells in skin aging, and it may play an important role in the balance of proliferation and differentiation. However, further studies are needed to determine the mechanism by which AQP5 regulates the proliferation and differentiation of epidermal skin cells in aging.

Detection of the small oligonucleotide products of nucleotide excision repair in UVB-irradiated human skin

UVB radiation results in the formation of potentially mutagenic photoproducts in the DNA of epidermal skin cells. In vitro approaches have demonstrated that the nucleotide excision repair (NER) machinery removes UV photoproducts from DNA in the form of small (∼30-nt-long), excised, damage-containing DNA oligonucleotides (sedDNAs). Though this process presumably takes place in human skin exposed to UVB radiation, sedDNAs have not previously been detected in human skin. Using surgically discarded human skin, we have optimized the detection of the sedDNA products of NER from small amounts of human epidermal tissue ex vivo within minutes of UVB exposure and after UVB doses that normally lead to minimal erythema. Moreover, sedDNA generation was inhibited by treatment of skin explants with spironolactone, which depletes the epidermis of the essential NER protein XPB to mimic the skin of xeroderma pigmentosum patients. Time course experiments revealed that a partially degraded form of the sedDNAs could be readily detected even 12 hours following UVB exposure, which indicates that these repair products are relatively stable in human skin epidermis. Together, these data suggest that sedDNA detection may be a useful assay for determining how genetic, environmental, and other factors influence NER activity in human skin epidermis and whether abnormal sedDNA processing contributes to photosensitive skin disorders.

Blue light disrupts the circadian rhythm and create damage in skin cells.

On a daily basis, the skin is exposed to many environmental stressors and insults. Over a 24-h natural cycle, during the day, the skin is focused on protection; while at night, the skin is focused on repairing damage that occurred during daytime and getting ready for the next morning. Circadian rhythm provides the precise timing mechanism for engaging those different pathways necessary to keep a healthy skin through clock genes that are present in all skin cells. The strongest clue for determining cellular functions timing is through sensing light or absence of light (darkness). Here, we asked the question if blue light could be a direct entrainment signal to skin cells and also disrupt their circadian rhythm at night. Through a reporter assay for per1 transcription, we demonstrate that blue light at 410nm decreases per1 transcription in keratinocytes, showing that epidermal skin cells can sense light directly and control their own clock gene expression. This triggers cells to "think" it is daytime even at nighttime. Elsewhere, we measured different skin cell damage because of blue light exposure (at different doses and times of exposure) vs. cells that were kept in full darkness. We show an increase in ROS production, DNA damage and inflammatory mediators. These deleterious effects can potentially increase overall skin damage over time and ultimately accelerates ageing.

YKL-40 Promotes Proliferation of Cutaneous T-Cell Lymphoma Tumor Cells through Extracellular Signal–Regulated Kinase Pathways

YKL-40, one of the chitinase-like proteins, is associated with the pathogenesis of a wide variety of human diseases through modulation of inflammation and tissue remodeling by its diverse roles in cell proliferation, differentiation, and survival. Emerging evidence shows that aberrantly expressed YKL-40 promotes the development of malignancies by inducing proliferation of tumor cells, cytokine production, and angiogenesis by acting on various stromal cells, immune cells, and tumor cells. In this study, we investigated the expression and function of YKL-40 in cutaneous T-cell lymphoma (CTCL). We first revealed that serum YKL-40 levels were increased in patients with CTCL and correlated with disease severity markers. We also found that YKL-40 was expressed by epidermal keratinocytes and tumor cells in lesional skin of CTCL by immunohistochemistry. Although YKL-40 did not affect cytokine production from CTCL cell lines, YKL-40 promoted the proliferation of Hut78 cells and HH cells invitro, which was dependent on extracellular signal-regulated kinase 1/2 pathways. Moreover, exogenous YKL-40 administration enhanced tumor growth of HH cells invivo. Our study has suggested that YKL-40 produced from epidermal keratinocytes and CTCL cells promoted the proliferation of CTCL cells through extracellular signal-regulated kinase 1/2 pathways in autocrine and paracrine manners, leading to development of CTCL.

Fluorescence imaging of Cys in keratinocytes upon UVB exposure using phenyl doped graphitic carbon nitride Nanosheets-Au nanoparticles nanocomposite

Ultraviolet B (UVB) irradiation induces the generation of reactive oxygen species (ROS) and causes damages to human skin. The depletion of glutathione (GSH) to scavenge ROS can protect skin cells from oxidative damage. However, little is known about the concentration level changes of cysteine (Cys), a precursor of GSH in skin cells after exposure to UVB irradiation. Herein, phenyl doped graphitic carbon nitride nanosheets-Au nanoparticles nanocomposite was prepared by in situ deposition of Au nanoparticles on the surface of phenyl doped graphitic carbon nitride nanosheets and showed a turn-on fluorescence response toward Cys over homocysteine, glutathione under physiological conditions. In the presence of Cys, remarkable enhancement of green fluorescence was observed. This nanocomposite was successfully applied for fluorescence imaging of Cys in human skin epidermal cells and monitoring the changes of Cys concentration level under the oxidative stress upon exposure to UVB irradiation in keratinocytes. It was found that the concentration of Cys was increased in the initial period after exposure to UVB irradiation and then gradually decreased to the normal level for the synthesis of GSH to defense the oxidative stress. Our result helps to understand the physiological function of Cys in human skin cells under UVB exposure.

Effect of alerce (Fitzroya cupressoides) cell culture extract on wound healing repair in a human keratinocyte cell line.

Fitzroya cupressoides, commonly known as alerce, is an endemic conifer unique to southern South America. Alerce wood is renowned for its durability and resistance to biological degradation due to the presence of a particular class of secondary metabolite. Alerce extracts have been used in traditional medicine for different skin lesion treatments. To develop a cell culture system to produce alerce extract and evaluate its cytotoxicity and effects on in vitro wound healing. Cell cultures and aqueous extracts were prepared from alerce needles. Cytotoxicity was evaluated in keratinocytes (HaCaT line) and melanocites (C32 line) using the XTT assay. Wound healing was assayed with the scratch test in HaCaT cells, using mitomycin C to evaluate the role of cell division in the wound closure. Alerce cell culture extract has a significant effect on wound healing at different concentrations. No positive effects on the viability of normal and cancerous skin cells were observed. These results suggest that alerce extracts stimulate cell division in human skin epidermal cells in the context of wound repair. Bioactive compounds extracted from alerce cell cultures show promise as ingredients in dermocosmetic formulations, but further clinical studies are required to support these findings at the tissue level.

Mechanism of SPRY1 methylation regulating natural aging of skin epidermal cells.

To investigate the relationship among natural aging of epidermal cells, epigenetics, and SPRY1 methylation mechanism. Immunohistochemistry, reverse transcription-PCR (RT-PCR), and Western blot were used to detect the expression of DNA methyltransferase 1 (DNMT1) and Sprouty1 (SPRY1) in skin epithelial cells from different age groups. An aging model of HaCaT cells was constructed. In HaCaT cells and their aging groups, DNMT1 and SPRY1 expression were detected by RT-PCR and WB. SPRY1 methylation status in epidermal cells from different age groups and HaCaT cells were detected by Methylation-Specific PCR (MS-PCR). The expression of DNMT1 and SPRY1 in skin epithelial cells from natural aging groups decreased with age; there was no significant difference in the expression of DNMT1 in HaCaT cells and the different age groups. The expression of SPRY1 in HaCaT cells was lower than it was in the aging groups. The methylation status of SPRY1 gradually decreased as the age of skin epidermal cells increased, while the methylation status of SPRY1 was not different between HaCaT cells and the aging group. DNMT1 is involved in the regulation of natural aging of skin epidermal cells but has a nominal role in our induced aging model. SPRY1 is involved in natural aging and induced aging of skin epidermal cells. The regulation of SPRY1 methylation is involved in the natural senescence of skin epidermal cells, while the induced aging of epidermal cells is nominally involved in the mechanism of SPRY1 methylation.

022 Crosstalk between vitiligo skin T-cell secretome and epidermal cell response

022 Crosstalk between vitiligo skin T-cell secretome and epidermal cell response

Laser versus dermabrasion and split thickness skin graft for management of post burn leucoderma

Background: The aim of the study is to compare between dermabrasion and split thickness skin grafting and fractional CO2 laser in management of post burn leucoderma. Deep burn can have serious aesthetic consequences as it often result in scar tissue and pigmentary changes in the skin. It is understood that skin pigmentation involves melanin. Leucoderma results from melanin loss at the basal layer of the epidermis. Fibrosis ultimately inhibits melanocyte migration and subsequent production of melanin in the injured area. Management of post burn leucoderma was either non-surgical or surgical treatment. Non-surgical therapies are make-up, tattooing and fractional CO2 laser. The surgical treatments include dermabrasion with thin split thickness skin grafting, non-cultured keratinocyte-melanocyte suspensions, mini grafting, cultured epithelium, blister epidermal grafting, chip skin grafting and epidermal cell suspension spray.Methods: A prospective study of 30 patients with post burn leucoderma between May 2018 and May 2019, at Ahmed Maher Teaching Hospital. Dermabrasion and split thickness skin grafting in 15 patients (group 1). Fractional CO2 laser in another 15 patients (group 2).Results: Group one: 13% of patients showed excellent colour match, 33% good colour match and 53% poor colour match. Group two: 27% of patients showed excellent colour match, 47% good colour match and 26% poor colour match (p value=0.311).Conclusions: Fractional CO2 laser is better than dermabrasion and STSG for management of post burn leucoderma.