Skin Of Acne Patients Research Articles

Integration of Single-Cell Transcriptomics Data Reveal Differences in Cell Composition and Communication in Acne.

Acne is a kind of hair follicle sebaceous inflammatory disease, which has a high incidence rate among adolescents. Comparative data on cells which beneficial for precise treatment of acne patients. After integrating and removing the batch effect of single-cell transcriptomics data of acne patients and health skin, the dimensionality reduction clustering was performed and the change in characteristics of each cell group were analyzed. Further, cell communication differences between gender were analyzed by use Cellchat software. 70,189 cells were analyzed, and 11 cell groups were identified. The proportion of basal cells and macrophages in skin of acne patients are relatively high than that of skin in healthy people. The results of cell communication showed that the communication intensity of acne patients was significantly higher than that of healthy skin, and the endothelial cells showed a strong ability to receive signals. From the perspective of gender differences, the proportion of macrophages in male patients were higher than that in female patients, and there were a large number of basal cells in the lesion area of female patients. There are also have some specific immune response ligand-receptor regulatory signals in male patients. There are significant differences in skin cell composition and cell communication patterns between acne patients and healthy people, especially reflected in gender differences. Basal cells, macrophages and endothelial cells can serve as key targets for acne treatment. The treatment methods for men and women should be more personalized.

1370 MTORC1 activity is increased in the skin of acne patients and is suppressed with isotretinoin treatment

1370 MTORC1 activity is increased in the skin of acne patients and is suppressed with isotretinoin treatment

Effects of mesotherapy introduction of compound glycyrrhizin injection on the treatment of moderate to severe acne.

Compound glycyrrhizin has achieved outstanding results in the treatment of various skin diseases. However, the use of mesotherapy to inject compound glycyrrhizin into the skin to treat acne is still understudied. This paper aims to explore the effects of mesotherapy introduction of compound glycyrrhizin injection on the acne. A total of 108 patients were included in this study and divided into the control group (n=54) and the observation group (n=54). The control group was treated with topical clindamycin gel, while the study group was treated with topical clindamycin gel + mesotherapy and compound glycyrrhizin injection. Skin transepidermal water loss (TEWL), cuticle water content, acne severity, adverse reactions, and inflammatory reactions were documented before and after treatment in the two groups. The usage of mesotherapy to inject compound glycyrrhizin into the skin of acne patients more effectively treat acne than traditional clindamycin gel. The mesotherapy compound glycyrrhizin can more effectively protect the skin barrier of patients and reduce the loss of skin moisture. Compared with the traditional clindamycin gel, the combination of mesotherapy and compound glycyrrhizin more effectively inhibit the inflammatory reaction in acne patients and reduce skin damage in acne patients. Mesoderm introduction of compound glycyrrhizin injection has better effects on the treatment of moderate to severe acne than clindamycin gel.

The role of proteins implicated in skin steroidogenesis in acne vulgaris development

Background. Acne vulgaris belongs to androgen-dependent diseases where androgens cause sebaceous gland hypertrophy with a subsequent enlargement of sebum production.
 Aims. Determination of the expression profile of steroidogenesis-related proteins in normal skin and skin of patients with acne.
 Material and methods. Immunohistochemical assay was carried out to characterize TSPO, StAR, CYP11A1, and 3-hydroxysteroid dehydrogenase expression in skin of patients with acne vulgaris and in normal skin.
 Results. Expression levels of a protein TSPO which is involved in a steroidogenesis-limited step was increased in mature sebocytes of acne vulgaris patients. StAR, CYP11A1, and 3-hydroxysteroid dehydrogenase immunovisualization was found both in normal skin and in the skin of acne patients.
 Conclusions. The revealed alterations in expression of steroidogenesis-related protein in acne skin may indicate not only the conversion of steroids produced by external steroidogenesis organs but elevated steroids local production as well. The fact may account both for sebaceous gland hyperplasia and inflammation sustenance in skin.

Skin dysbiosis and Cutibacterium acnes biofilm in inflammatory acne lesions of adolescents

Acne vulgaris is a common inflammatory disorder affecting more than 80% of young adolescents. Cutibacterium acnes plays a role in the pathogenesis of acne lesions, although the mechanisms are poorly understood. The study aimed to explore the microbiome at different skin sites in adolescent acne and the role of biofilm production in promoting the growth and persistence of C. acnes isolates. Microbiota analysis showed a significantly lower alpha diversity in inflammatory lesions (LA) than in non-inflammatory (NI) lesions of acne patients and healthy subjects (HS). Differences at the species level were driven by the overabundance of C. acnes on LA than NI and HS. The phylotype IA1 was more represented in the skin of acne patients than in HS. Genes involved in lipids transport and metabolism, as well as potential virulence factors associated with host-tissue colonization, were detected in all IA1 strains independently from the site of isolation. Additionally, the IA1 isolates were more efficient in early adhesion and biomass production than other phylotypes showing a significant increase in antibiotic tolerance. Overall, our data indicate that the site-specific dysbiosis in LA and colonization by virulent and highly tolerant C. acnes phylotypes may contribute to acne development in a part of the population, despite the universal carriage of the microorganism. Moreover, new antimicrobial agents, specifically targeting biofilm-forming C. acnes, may represent potential treatments to modulate the skin microbiota in acne.

Evaluation of PPARγ expression in skin of acne patients

Acne is a chronic disease of the pilosebaceous unit. Much attention is paid to the pathogenesis and optimization of acne therapy. Evidence is emerging about the role of PPARγ receptors in maintaining inflammation and increasing sebum production, as well as an indirect role in the development of pruritus, which may allow for a correlation between the severity of inflammation in acne, the prevalence of pruritus, and the influence of PPARγ receptor expression on these processes.

27862 Trifarotene transcriptomics analysis and acne-related gene expression

Trifarotene cream, 0.005% is an FDA approved topical retinoid indicated for treatment of facial and truncal acne and has received positive outcome through the European Decentralized Procedure. Trifarotene is the first novel topical retinoid molecule approved for acne treatment in 20 years, and the only approved retinoid that specifically acts through retinoic acid receptor gamma. This study investigated new potential pathways through which trifarotene exerts its efficacy in acne by analyzing the changes in gene expression in the skin of acne patients. Subjects with moderate inflammatory acne of the back were treated with trifarotene 0.005% or vehicle cream on dedicated back areas for 27 days, and 4 biopsies were collected on each subject (non-involved skin, acne papule, trifarotene, and vehicle-treated site). Large-scale gene expression profiling of the biopsies was performed using Affymetrix technology, and treatment specific gene expression profiles were generated using statistical modeling. This analysis highlighted a specific gene expression profile, comprising of 67 genes uniquely driven by Trifarotene treatment with most of these genes known to affect immune responses as well as extracellular matrix reorganization. Interestingly, those genes were downregulated as compared with the papule signature suggesting that trifarotene reverses some inflammatory processes of the papule. Altogether, these results show that trifarotene has a unique action in acne treatment by acting on epidermal differentiation and proliferation (Aubert et al., 2018) as well as on innate and adaptive immune cells in acne pathogenesis.

Probióticos y prebióticos: ¿beneficio real en dermatología?

Probiotics are defined as live microorganisms that, when administered in adequate amounts, confer a health benefit to the host beyond their nutritional contribution. In addition to their effects on gut homeostasis, probiotics may also regulate systemic immune and inflammatory responses. Therefore, modulating the gut microbiota by orally administered probiotics could exert positive effects on the skin. The cutaneous disease in which these effects have been most widely studied is atopic dermatitis, and greater benefits have been obtained in the prevention than in the treatment of this entity. Prebiotics, in contrast, are non-digestible food ingredients that beneficially affect the host by selectively stimulating bacterial growth and/or activity. This concept was originally developed to selectively modify the gut microflora, but in principle could be applied to modulate the composition of any microbial community, including the skin microflora. A prominent example is the skin of acne patients, in which prebiotic administration could be effective in reducing the amount of Propionibacterium acnes, and at the same time in preserving or even stimulating the growth of beneficial bacteria. Continued research is required before solid, evidence-based recommendations can be made.

Temporal changes in gene expression in the skin of patients treated with isotretinoin provide insight into its mechanism of action

Isotretinoin (13-cis RA) is the most potent agent in the treatment of acne. Insights into its mechanism of action can lead to drug discovery of alternative compounds with comparable efficacy but improved safety. The goal of this study is to compare the temporal changes in gene expression in the skin of acne patients after 1 week and 8 weeks of treatment with isotretinoin. Microarray analysis was performed on skin biopsies taken from eight acne patients prior to and at 8 weeks of treatment with isotretinoin. Results were compared with data obtained from seven acne patients biopsied at one week of treatment in a prior study. Distinctly different patterns of gene expression were noted. At 8 weeks, genes encoding extracellular matrix proteins were upregulated and numerous genes encoding lipid metabolizing enzymes were downregulated. At 1 week, genes encoding differentiation markers, tumor suppressors and serine proteases were upregulated. Only three genes were commonly downregulated. The temporal changes in gene expression in patient skin noted with isotretinoin substantiate many previously reported effects of isotretinoin and other retinoids, suggesting a model wherein isotretinoin induces apoptosis leading to reduced sebaceous gland size, decreased expression of lipid metabolizing enzymes and increased matrix remodeling during acne resolution.

Prevalence of antibiotic-resistant propionibacteria on the skin of acne patients: 10-year surveillance data and snapshot distribution study.

Cutaneous propionibacteria are implicated in acne pathogenesis, although their exact role in the genesis of inflammation is still poorly understood. Agents, including antibiotics, that reduce the numbers of propionibacteria on skin are therapeutic. Resistance in the target organism is a well-recognized consequence of antibiotic therapy for acne but formal prevalence and distribution data are lacking. To monitor the prevalence of skin colonization by antibiotic-resistant propionibacteria in acne patients attending the dermatology out-patient clinic at Leeds General Infirmary over a 10-year period beginning in 1991, and to examine the distribution of resistant strains on acne-prone skin and in the nares. Propionibacterial samples were obtained from the skin surface of the worst affected site (usually the face) of 4274 acne patients using a moistened swab. The swab was used to inoculate agar plates with and without selective antibiotics. After anaerobic incubation at 37 degrees C for 7 days, the amount of growth in the presence of each antibiotic was scored on a scale from 0 to 5+. A small number of patients (72) were selected for more detailed quantitative sampling at six different sites to examine the distribution of resistant propionibacteria on acne-prone skin and in the anterior nares. The proportion of patients carrying strains resistant to one or more commonly used antiacne antibiotics rose steadily from 34.5% in 1991 to a peak of 64% in 1997. The prevalence dropped to 50.5% during 1999 and then rose again to 55.5% in 2000. Resistance to erythromycin was the most common and the majority of erythromycin-resistant strains were cross-resistant to clindamycin. Resistance to tetracyclines was less common in all years and with little increase over time. The more detailed quantitative study in 72 patients showed that population densities of resistant propionibacteria varied considerably between sites and between individuals. Almost invariably, patients were colonized with resistant strains at multiple sites, including the nares. Skin colonization with antibiotic-resistant propionibacteria is much more common now than a decade ago. Resistant propionibacteria are widely distributed on acne-prone skin and in the nares. This suggests that they will be very difficult to eradicate using existing therapeutic regimens, especially from the nasal reservoir.

Phenotypic and genotypic characterization of antibiotic-resistant Propionibacterium acnes isolated from acne patients attending dermatology clinics in Europe, the U.S.A., Japan and Australia.

Propionibacterium acnes is the target of antimicrobial treatments for acne vulgaris. Acquired resistance to erythromycin, clindamycin and tetracyclines has been reported in strains from diverse geographical loci, but the molecular basis of resistance, via mutations in genes encoding 23S and 16S rRNA, respectively, has so far only been elucidated for isolates from the U.K. To determine whether similar or different resistance mechanisms occur in resistant P. acnes isolates from outside the U.K. The phenotypes and genotypes of 73 antibiotic-resistant strains of P. acnes obtained from the skin of acne patients in the U.K., U.S.A., France, Germany, Australia and Japan were compared. Antibiotic susceptibilities were determined by minimum inhibitory concentration (MIC) measurements, and polymerase chain reaction and DNA sequencing were used to identify mutations in genes encoding rRNA. Most erythromycin-resistant isolates (MIC(90) > or = 512 microg mL(-1)) were cross-resistant to clindamycin but at a much lower level (MIC(90) > or = 64 microg mL(-1)). As in the U.K., resistance to erythromycin was associated with point mutations in 23S rRNA in 49 of 58 strains. An A-->G transition at Escherichia coli equivalent base 2058 was present in 24 strains. This gave a unique cross-resistance phenotype against a panel of macrolide, lincosamide and type B streptogramin antibiotics. Two further point mutations (at E. coli equivalent bases 2057 and 2059) were identified (in three and 22 isolates, respectively) and these were also associated with specific cross-resistance patterns originally identified in isolates from the U.K. However, nine of 10 erythromycin resistant-strains from Germany did not exhibit any of the three base mutations identified and, in six cases, cross-resistance patterns were atypical. Consistent with previous U.K. data, 34 of 38 tetracycline-resistant strains carried a base mutation at E. coli 16S rRNA equivalent base 1058. Tetracycline-resistant isolates displayed varying degrees of cross-resistance to doxycycline and minocycline, but isolates from the U.S.A. had higher MICs for minocycline (4--16 microg mL(-1)) than isolates from other countries and, in particular, Australia. All the P. acnes isolates resistant to one or more of the commonly used antiacne antibiotics were sensitive to penicillin, fusidic acid, chloramphenicol and the fluoroquinolone, nadifloxacin. All but one isolate (from the U.K.) were sensitive to trimethoprim. This study shows that 23S and 16S mutations identified in the U.K. conferring antibiotic resistance in P. acnes are distributed widely. However, resistant strains were isolated in which mutations could not be identified, suggesting that as yet uncharacterized resistance mechanisms have evolved. This is the first report of high-level resistance to minocycline and is of concern as these strains are predicted to be clinically resistant and are unlikely to remain confined to the U.S.A. Epidemiological studies are urgently required to monitor how resistant strains are selected, how they spread and to ascertain whether the prevalence of resistance correlates with antibiotic usage patterns in the different countries.

The effects of acne treatment with a combination of benzoyl peroxide and erythromycin on skin carriage of erythromycin resistant propionibacteria

Concomitant application of 5% w/w benzoyl peroxide and 3% w/w erythromycin has previously been shown to prevent the overgrowth, on the skin of acne patients, of erythromycin-resistant coagulase-negative staphylococci, which occurs when the antibiotic is used alone. Two in vivo studies were carried out to assess the ability of the same therapeutic combination to inhibit the growth of pre-existing erythromycin-resistant propionibacteria and to prevent the selection of resistant strains during treatment. A double-blind clinical trial in 37 patients with mild to moderate acne vulgaris showed that the combination brought about a > 3 log10 c.f.u. reduction in total propionibacterial numbers/cm2 after 6 weeks therapy (P < 0.001, Wilcoxon's matched pairs) and also significantly reduced the number of erythromycin-resistant propionibacteria (P < 0.05). In contrast, erythromycin alone reduced the total propionibacterial count by < 1.5 log10 c.f.u./cm2 after 6 weeks (P < 0.05) and did not affect the number of erythromycin-resistant strains. The combined formulation was significantly more effective at reducing total propionibacterial numbers at 6 (P < 0.01, Mann-Whitney) and 12 weeks (P < 0.05) than erythromycin alone, although, after 12 weeks, the anti-propionibacterial efficacy of both preparations was less marked. Five patients on combination therapy, and five treated with erythromycin alone, acquired erythromycin-resistant strains de novo at week 6 or week 12. In an open study in 21 acne patients, who each carried > 10(3) c.f.u. erythromycin-resistant propionibacteria/cm2 skin pretreatment, the combination of erythromycin and benzoyl peroxide reduced the total propionibacterial count by > 2.5 log10 and the number of erythromycin-resistant strains by a similar amount (P < 0.001, Wilcoxon). This was accompanied by highly significant reductions in acne grade and lesion counts (P < 0.001). These data suggest that the combination of 5% w/w benzoyl peroxide and 3% w/w erythromycin has greater in vivo anti-propionibacterial activity than 3% w/w erythromycin alone, and brings about significant clinical improvement in acne patients with high numbers of erythromycin-resistant propionibacterial strains pretreatment.

Effects of benzoyl peroxide and erythromycin alone and in combination against antibiotic-sensitive and -resistant skin bacteria from acne patients

Topical formulations of erythromycin and benzoyl peroxide are popular and effective treatments for mild to moderate acne vulgaris. Use of the former is associated with resistance gain in both skin propionibacteria and coagulase-negative staphylococci, whereas use of the latter is not. We evaluated the efficacy of a combination of erythromycin and benzoyl peroxide against a total of 40 erythromycin-sensitive and -resistant strains of Staphylococcus epidermidis and skin propionibacteria in vitro. Using the checkerboard technique, five erythromycin resistant strains of Propionibacterium acnes were inhibited synergistically or additively by the combination. Complete mutual indifference was exhibited between the drugs against the remaining 35 strains. However, erythromycin resistant staphylococci and propionibacteria were inhibited by the same concentration of benzoyl peroxide as erythromycin-sensitive strains. These results suggest that, although the combination of erythromycin and benzoyl peroxide is not synergistic against the majority of erythromycin-resistant staphylococci and propionibacteria, the concomitant therapeutic use of both drugs should counteract the selection of erythromycin-resistant variants and reduce the number of pre-existing resistant organisms on the skin of acne patients.

Inhibition of erythromycin-resistant propionibacteria on the skin of acne patients by topical erythromycin with and without zinc

Propionibacteria resistant to high concentrations of erythromycin [minimal inhibitory concentration (MIC) > or = 0.5 mg/ml] are now commonly isolated from the skin of antibiotic-treated acne patients. This double-blind study was carried out to assess the ability of 4% w/v erythromycin with and without 1.2% w/v zinc acetate to reduce the numbers of erythromycin-resistant propionibacteria in vivo, and also to monitor the acquisition of resistant strains de novo during therapy. Under laboratory conditions, erythromycin-resistant propionibacteria were shown to be as sensitive to zinc acetate as fully sensitive strains. In vivo, the erythromycin/zinc complex and erythromycin alone produced highly significant reductions in total propionibacteria (P < 0.001) and in the number of erythromycin-resistant strains (P < 0.001 at 8 weeks). After 12 weeks, resistant propionibacteria were reacquired, or acquired de novo, by three patients treated with erythromycin alone and four patients treated with the erythromycin/zinc complex. In contrast, changes in numbers of Micrococcaceae were slight and, after 12 weeks, erythromycin-resistant strains were predominant in both treatment groups. In vitro MIC determinations suggested that this finding might be explained by the exceptionally high degree of erythromycin resistance displayed by some staphylococcal strains (MIC > 4 mg/ml) and by the relative insensitivity of all staphylococcal strains to zinc acetate. Erythromycin with and without zinc was clinically effective, and both preparations produced significant reductions in acne grade, and inflamed and non-inflamed lesion counts (P < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Vitamin A in skin and serum--studies of acne vulgaris, atopic dermatitis, ichthyosis vulgaris and lichen planus.

The concentrations of vitamin A and total carotenoids were measured in serum and skin of 61 patients with acne vulgaris, atopic dermatitis, ichthyosis vulgaris or lichen planus, and compared with those in 37 healthy subjects. The mean serum concentrations of retinol and retinol-binding protein were significantly decreased in patients with acne (P less than 0.01) and slightly increased in those with ichthyosis (P less than 0.05), but were otherwise normal. Serum carotenoid levels did not differ between patients and controls. Superficial shave biopsies from both involved and uninvolved skin were examined for the presence of retinol (vitamin A1), dehydroretinol (vitamin A2) and total carotenoids. The mean retinol concentration was increased in lichen planus lesions (P less than 0.05) and decreased in both acne skin (involved and uninvolved) and in lesions of atopic dermatitis (P less than 0.05). The mean dehydroretinol concentration was markedly increased in lesions of atopic dermatitis and lichen planus (P less than 0.01). No consistent abnormalities were found in skin of patients with ichthyosis vulgaris. The mean carotenoid concentration in the patients' skin did not differ significantly from that in the controls. The reduced retinol level in the skin of acne patients is probably explained by diminished supply of vitamin A from the blood. The abnormal ratio of retinol to dehydroretinol in lesions of lichen planus and atopic dermatitis is possibly due to changes in cutaneous vitamin A metabolism associated with epidermal hyperproliferation and inflammation.