Epithelial Resurfacing: The Bronchial Skin Peel.
Ontology highlight
ABSTRACT:
SUBMITTER: Shah PL
PROVIDER: S-EPMC7462398 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Non-melanoma skin cancer is a disease primarily afflicting geriatric patients as evidenced by the fact that 80% of all non-melanoma skin cancers are diagnosed in patients over the age of 60 years. As such, geriatric skin responds to cancer-inducing UVB irradiation in a manner that allows the establishment of tumor cells. Currently, the only effective treatment for non-melanoma skin cancer is the removal of the tumors after they appear, indicating the need for a more cost-effective prophylactic therapy. Geriatric volunteers were treated with fractionated laser resurfacing therapy on either sun-protected (upper buttocks) or chronically sun-exposed (dorsal forearm) skin. Fractionated laser resurfacing therapy was shown to decrease the occurrence of senescent fibroblasts in geriatric dermis, increase the dermal expression of IGF-1, and correct the inappropriate UVB response observed in untreated geriatric skin. These responses to fractionated laser resurfacing were equal to the effects seen previously using the more aggressive wounding following dermabrasion. Furthermore, fractionated laser resurfacing was equally effective in both sun-protected and sun-exposed skin. The ability of fractionated laser resurfacing treatment to protect against the occurrence of UVB-damaged proliferating keratinocytes indicates the potential of fractionated laser resurfacing to reduce or prevent aging-associated non-melanoma skin cancer.
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Project description:Eosinophilic inflammation and remodeling of the airways including subepithelial fibrosis and myofibroblast hyperplasia are characteristic pathological findings of bronchial asthma. Epithelial to mesenchymal transition (EMT) plays a critical role in airway remodelling. In this study, we hypothesized that infiltrating eosinophils promote airway remodelling in bronchial asthma. To demonstrate this hypothesis we evaluated the effect of eosinophils on EMT by in vitro and in vivo studies. EMT was assessed in mice that received intra-tracheal instillation of mouse bone marrow derived eosinophils and in human bronchial epithelial cells co-cultured with eosinophils freshly purified from healthy individuals or with eosinophilic leukemia cell lines. Intra-tracheal instillation of eosinophils was associated with enhanced bronchial inflammation and fibrosis and increased lung concentration of growth factors. Mice instilled with eosinophils pre-treated with transforming growth factor(TGF)-?1 siRNA had decreased bronchial wall fibrosis compared to controls. EMT was induced in bronchial epithelial cells co-cultured with human eosinophils and it was associated with increased expression of TGF-?1 and Smad3 phosphorylation in the bronchial epithelial cells. Treatment with anti-TGF-?1 antibody blocked EMT in bronchial epithelial cells. Eosinophils induced EMT in bronchial epithelial cells, suggesting their contribution to the pathogenesis of airway remodelling.
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Project description:Despite their great potential, medium and deep trichloroacetic acid peels are underused in light-skinned patients and are rarely used in darker-skinned patients because of the widespread fear of pigmentary complications and scarring. This concern has led many physicians to opt for the use of lighter types of peels (glycolic acid peel, Jessner peel, etc) and different lasers and intense light technologies. Trichloroacetic acid peels have been described in numerous publications. However, no study to date has described the precise technique and the practical pearls of a successful trichloroacetic acid peel approach in a clear, detailed, and reproducible manner.To clarify a practical approach to a universal trichloroacetic acid peel and to offer novice and experienced facial plastic surgeons an organized, easy, and safe technique for medium and deep trichloroacetic acid peels.This study was a case series of universal trichloroacetic acid peels in an academic setting. The study dates were January 1, 1996, to November 1, 2015.This article discusses the preoperative evaluation for a chemical peel, a previously published genetico-racial skin classification, and the trichloroacetic acid peel technique, which aims at standardizing and controlling the application of the acid to improve results and lessen complications. The "strip" technique is described, which increases the physician's control over the peel depth.A total of 923 trichloroacetic acid peels in 803 female patients (87.0%) and 120 male patients (13.0%) were reviewed (mean age, 41.59 years). The follow-up period ranged from 6 months to 13 years (mean, 13 months). This case series revealed a low incidence of complications, including 54 patients (5.9%) with persistent hyperpigmentation, 3 patients (0.3%) with mild telangiectasia, 2 patients (0.2%) with acute herpesvirus infection, 2 patients (0.2%) with bacterial Staphylococcus infection, and 1 patient (0.1%) with hypopigmentation.When properly applied, trichloroacetic acid peels are efficient and safe for light and dark skin. The technique can be an easily implementable addition to a physician's cosmetic practice.4.
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Project description:Respiratory epithelial cells are important for pulmonary innate immune responses during Pseudomonas aeruginosa infection. Tet methylcytosine dioxygenase 2 (Tet2) has been implicated in the regulation of host defense by myeloid and lymphoid cells, but whether Tet2 also contributes to epithelial responses during pneumonia is unknown. The aim of this study was to investigate the role of bronchial epithelial Tet2 in acute pneumonia caused by P. aeruginosa To this end, we crossed mice with Tet2 flanked by two Lox-P sites (Tet2fl/fl mice) with mice expressing Cre recombinase under the bronchial epithelial cell-specific Cc10 promoter (Cc10Cre mice) to generate bronchial epithelial cell-specific Tet2-deficient (Tet2fl/fl Cc10Cre ) mice. Six hours after infection with P. aeruginosa,Tet2fl/fl Cc10Cre and wild-type mice had similar bacterial loads in bronchoalveolar lavage fluid (BALF). At this time point, Tet2fl/fl Cc10Cre mice displayed reduced mRNA levels of the chemokines Cxcl1, Cxcl2, and Ccl20 in bronchial brushes. However, Cxcl1, Cxcl2, and Ccl20 protein levels and leukocyte recruitment in BALF were not different between groups. Tet2fl/fl Cc10Cre mice had increased protein levels in BALF after infection, indicating a disturbed epithelial barrier function, which was corroborated by reduced mRNA expression of tight junction protein 1 and occludin in bronchial brushes. Differences detected between Tet2fl/fl Cc10Cre and wild-type mice were no longer present at 24 h after infection. These results suggest that bronchial epithelial Tet2 contributes to maintaining epithelial integrity by enhancing intracellular connections between epithelial cells during the early phase of P. aeruginosa pneumonia.
| S-EPMC7927922 | biostudies-literature
Project description:Epithelial cells (EC) lining the most inner layers of secretory glands in Citrus peel are hypothesized to be the specialized cells that synthesize citrus essential oil. The major biosynthetic pathway(s) for essential oil are therefore postulated to be specifically and highly active in EC; transcripts that are involved in the pathway(s) are expected to be highly up-regulated in the cells as well. We performed cell-specific transcriptional analysis using GeneChip Citrus Genome Arrays to probe the global gene expression in EC during initial stage of essential oil biosynthesis and to identify groups of highly expressed genes in the EC. Grapefruits of two different sizes (diameters at 28 mm and 41 mm), at which points where biosynthesis of essential oil entering its active phase, were selected for the purpose of this experiment. For comparison, we selected parenchyma cells (PC), the non-oil-biosynthesizing cells, as the control cell type. Grapefruit peels were fixed, embedded in paraffin, sectioned and mounted on slides prior to cells isolation using laser microdissection and pressure catapulting. RNA was extracted from the isolated cells and then used for microarray hybridization. Transcriptional analysis were carried out by comparing transcript profiles between different cell types of the same time points, and same cell type at the different time points.
2012-04-18 | E-GEOD-33964 | biostudies-arrayexpress
Project description:BACKGROUND:Genome-wide association studies (GWASs) have identified various genes associated with asthma, yet, causal genes or single nucleotide polymorphisms (SNPs) remain elusive. We sought to dissect functional genes/SNPs for asthma by combining expression quantitative trait loci (eQTLs) and GWASs. METHODS:Cis-eQTL analyses of 34 asthma genes were performed in cells from human bronchial epithelial biopsy (BEC, n = 107) and from bronchial alveolar lavage (BAL, n = 94). RESULTS:For TSLP-WDR36 region, rs3806932 (G allele protective against eosinophilic esophagitis) and rs2416257 (A allele associated with lower eosinophil counts and protective against asthma) were correlated with decreased expression of TSLP in BAL (P = 7.9 × 10(-11) and 5.4 × 10(-4) , respectively) and BEC, but not WDR36. Surprisingly, rs1837253 (consistently associated with asthma) showed no correlation with TSLP expression levels. For ORMDL3-GSDMB region, rs8067378 (G allele protective against asthma) was correlated with decreased expression of GSDMB in BEC and BAL (P = 1.3 × 10(-4) and 0.04) but not ORMDL3. rs992969 in the promoter region of IL33 (A allele associated with higher eosinophil counts and risk for asthma) was correlated with increased expression of IL33 in BEC (P = 1.3 × 10(-6) ) but not in BAL. CONCLUSIONS:Our study illustrates cell-type-specific regulation of the expression of asthma-related genes documenting SNPs in TSLP, GSDMB, IL33, HLA-DQB1, C11orf30, DEXI, CDHR3, and ZBTB10 affect asthma risk through cis-regulation of its gene expression. Whenever possible, disease-relevant tissues should be used for transcription analysis. SNPs in TSLP may affect asthma risk through up-regulating TSLP mRNA expression or protein secretion. Further functional studies are warranted.
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Project description:Chronic obstructive pulmonary disease (COPD) is characterized by airway inflammation, small airway remodeling, and emphysema. Airway remodeling in patients with COPD involves both the airway epithelium and the subepithelial extracellular matrix (ECM). However, it is currently unknown how epithelial remodeling in COPD airways depends on the relative influence from inherent defects in the epithelial cells and alterations in the ECM. To address this, we analyzed global gene expression in COPD human bronchial epithelial cells (HBEC) and normal HBEC after repopulation on decellularized bronchial scaffolds derived from patients with COPD or donors without COPD. COPD HBEC grown on bronchial scaffolds showed an impaired ability to initiate ciliated-cell differentiation, which was evident on all scaffolds regardless of their origin. In addition, although normal HBEC were less affected by the disease state of the bronchial scaffolds, COPD HBEC showed a gene expression pattern indicating increased proliferation and a retained basal-cell phenotype when grown on COPD bronchial scaffolds compared with normal bronchial scaffolds. By using mass spectrometry, we identified 13 matrisome proteins as being differentially abundant between COPD bronchial scaffolds and normal bronchial scaffolds. These observations are consistent with COPD pathology and suggest that both epithelial cells and the ECM contribute to epithelial-cell remodeling in COPD airways.
| S-EPMC8399573 | biostudies-literature
Project description:Epithelial cells (EC) lining the most inner layers of secretory glands in Citrus peel are hypothesized to be the specialized cells that synthesize citrus essential oil. The major biosynthetic pathway(s) for essential oil are therefore postulated to be specifically and highly active in EC; transcripts that are involved in the pathway(s) are expected to be highly up-regulated in the cells as well. We performed cell-specific transcriptional analysis using GeneChip Citrus Genome Arrays to probe the global gene expression in EC during initial stage of essential oil biosynthesis and to identify groups of highly expressed genes in the EC.
2012-04-19 | GSE33964 | GEO
Project description:Airway epithelial mucus hypersecretion and mucus plugging are prominent pathologic features of chronic inflammatory conditions of the airway (e.g. asthma and cystic fibrosis) and in most of these conditions, women have worse prognosis compared with male patients. We thus investigated the effects of estradiol on mucus expression in primary normal human bronchial epithelial cells from female donors grown at an air liquid interface (ALI). Treatment with estradiol in physiological ranges for 2 weeks caused a concentration-dependent increase in the number of PAS-positive cells (confirmed to be goblet cells by MUC5AC immunostaining) in ALI cultures, and this action was attenuated by estrogen receptor beta (ER-β) antagonist. Protein microarray data showed that nuclear factor of activated T-cell (NFAT) in the nuclear fraction of NHBE cells was increased with estradiol treatment. Estradiol increased NFATc1 mRNA and protein in ALI cultures. In a human airway epithelial (1HAE0) cell line, NFATc1 was required for the regulation of MUC5AC mRNA and protein. Estradiol also induced post-translational modification of mucins by increasing total fucose residues and fucosyltransferase (FUT-4, -5, -6) mRNA expression. Together, these data indicate a novel mechanism by which estradiol increases mucus synthesis in the human bronchial epithelium.
| S-EPMC4070981 | biostudies-literature
Project description:IntroductionInterstitial lung abnormalities (ILA) often represent early fibrotic changes that can portend a progressive fibrotic phenotype. In particular, the fibrotic subtype of ILA is associated with increased mortality and rapid decline in lung function. Understanding the differential gene expression that occurs in the lungs of participants with fibrotic ILA may provide insight into development of a useful biomarker for early detection and therapeutic targets for progressive pulmonary fibrosis.MethodsMeasures of ILA and gene expression data were available in 213 participants in the Detection of Early Lung Cancer Among Military Personnel (DECAMP1 and DECAMP2) cohorts. ILA was defined using Fleischner Society guidelines and determined by sequential reading of computed tomography (CT) scans. Primary analysis focused on comparing gene expression in ILA with usual interstitial pneumonia (UIP) pattern with those with no ILA.ResultsILA was present in 51 (24%) participants, of which 16 (7%) were subtyped as ILA with a UIP pattern. One gene, pro platelet basic protein (PPBP) and seventeen pathways (e.g. TNF-α signalling) were significantly differentially expressed between those with a probable or definite UIP pattern of ILA compared to those without ILA. 16 of these 17 pathways, but no individual gene, met significance when comparing those with ILA to those without ILA.ConclusionOur study demonstrates that abnormal inflammatory processes are apparent in the bronchial airway gene expression profiles of smokers with and without lung cancer with ILA. Future studies with larger and more diverse populations will be needed to confirm these findings.
| S-EPMC10566143 | biostudies-literature