IntroductionThe aim of this study was to investigate the distribution of antimicrobial susceptibility, biotypes and phylotypes of clinical Cutibacterium acnes (C. acnes, formerly Propionibacterium acnes) isolates as well as the relationship among demographic factors, C. acnes biotypes and phylotypes.MethodsCutibacterium acnes was collected from the skin lesions of acne patients who visited the dermatologic department of Huashan Hospital in Shanghai from October 2016 to March 2017. The agar dilution method was conducted to determine the minimum inhibitory concentrations (MICs) of C. acnes, the fermentation test to identify biotypes and then multiplex touchdown polymerase chain reaction (PCR) to identify phylotypes.ResultsOf the 63 C. acnes strains we isolated, 18 (28.6%), 31 (49.2%) and 4 (6.3%) strains were resistant to clindamycin, erythromycin and moxifloxacin, respectively; no strains were resistant to tetracycline, minocycline, fusidic acid or β-lactam, while metronidazole was completely resisted; 3 strains showed multidrug resistance (MDR). Biotype III (BIII) was the major biotype (50.8%) followed by BI and BV (both 15.9%), BII (12.7%) and lastly BIV (4.8%). IA1 was the predominant phylotype (71.4%) followed by IA2 (19.0%), II (4.8%), IB (3.2%) and IC (1.6%), while III was not detected. Significant differences were observed in the severity of disease: different degrees of acne severity reflected different biotype and phylotype distributions, and the biotype distribution of mild acne was different from that of moderate acne; the phylotype distribution of moderate acne varies from that of severe acne, too. Additionally, there was no significant difference in the distribution of biotypes or phylotypes between resistant and susceptible strains.ConclusionErythromycin and clindamycin resistances are the most common in clinical C. acnes strains; BIII is the predominant biotype and IA1 is the major phylotype of C. acnes, which are mainly related to disease severity.

No abstract

Background The anti-inflammatory effect of glycyrrhizin has been widely recognized, while the specific mechanism of glycyrrhizin in psoriasis remains poorly understood. Results In the imiquimod-induced mouse model of psoriasis (IMD), we found that glycyrrhizin can substantially improve the adverse symptoms in mice. The hematoxylin-eosin staining results showed that glycyrrhizin can also improve the pathological state of skin cells in IMD mice. Using enzyme-linked immunosorbent assay (ELISA), we found that glycyrrhizin substantially inhibited the expression of IL-17A and IFN-γ in the serum of IMD mice. In order to simulate the effect of IL-17A on keratinocytes in psoriasis, we treated HaCaT cells with 100 ng/mL IL-17A (IL-17A-HaCaT cells) for 48 h. Then, using cell-counting kit-8 (CCK-8) and ELISA assays, we found that glycyrrhizin inhibited the proliferation of IL-17A-HaCaT cells and reversed the promotion of IL-6, CCL20, and TNF-α induced by IL-17A. Further, western blotting (WB) results indicated that glycyrrhizin promoted the expression of SIRT1 and inhibited the expression of STAT3 and phosphorylated STAT3 (p-STAT3). By treating IL-17A-HaCaT cells with EX-527 (a potent and selective inhibitor of SIRT1), combined with CCK-8 and WB experiments, we initially found that EX-527 inhibited the proliferation of IL-17A-HaCaT cells and promoted the expression of STAT3, p-STAT3, and acetylated STAT3 (a-STAT3). However, when glycyrrhizin was added at the same time, the proliferation of IL-17A-HaCaT cells increased, and the expression of STAT3, p-STAT3, and a-STAT3 reduced. We then knocked down the expression of SIRT1 via small interfering RNA in IL-17A-HaCaT cells, and the results were consistent with those of EX-527. Conclusions Together, these results indicated that glycyrrhizin improved psoriasis by inhibiting the expression of IL-17A and IFN-γ in vivo and suppressed the proliferation of IL-17A-HaCaT cells and the expression of STAT3, p-STAT3, and a-STAT3 by upregulating SIRT1 in vitro.