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皮肤共生菌表皮葡萄球菌促进携带紫外线 B 诱导的 DNA 损伤的黑素细胞的存活,而痤疮丙酸杆菌通过增加细胞凋亡抑制黑素细胞的存活。

Skin commensal bacteria Staphylococcus epidermidis promote survival of melanocytes bearing UVB-induced DNA damage, while bacteria Propionibacterium acnes inhibit survival of melanocytes by increasing apoptosis.

机构信息

Department of Dermatology, University of California, San Diego, California.

出版信息

Photodermatol Photoimmunol Photomed. 2018 Nov;34(6):405-414. doi: 10.1111/phpp.12411. Epub 2018 Jul 23.

DOI:10.1111/phpp.12411
PMID:29974533
Abstract

BACKGROUND/PURPOSE: Skin commensal bacteria have been described to help orchestrate skin homeostasis, signaling through innate immunity pathways. This study for the first time aimed at studying the relationship between skin commensals and melanocytes after UVB exposure.

METHODS

An in vitro UVB radiation model with normal human epidermal melanocytes (NHMs) and skin commensal bacteria supernatant from Staphylococcus epidermidis and Propionibacterium acnes was established. Melanocytes DNA damage, cyclobutane pyrimidine dimers (CPD), and cellular proliferation marker Ki-67 were measured by ELISA and immunofluorescence staining. Cell apoptosis was assessed by flow cytometry and PCR array and RT-qPCR.

RESULTS

Normal human epidermal melanocytes are able to survive and proliferate while bearing DNA damage after UVB radiation. Skin commensal bacteria S. epidermidis and its by-product LTA promote melanocytes survival by inducing upregulation of TRAF1, CASP14, CASP5, and TP73. On the other hand, P. acnes can inhibit UVB-irradiated melanocytes survival by increasing apoptosis.

CONCLUSION

Our studies show different aspects of commensal activity on melanocytes during irradiation. The possible balance achieved by the different skin commensal can influence NHM potential to become cancer cells.

摘要

背景/目的:皮肤共生菌已被描述为有助于协调皮肤的稳态,通过先天免疫途径发出信号。本研究首次旨在研究 UVB 照射后皮肤共生菌与黑素细胞之间的关系。

方法

建立了含有正常人体表皮黑素细胞(NHM)和来自表皮葡萄球菌和痤疮丙酸杆菌的皮肤共生菌上清液的体外 UVB 辐射模型。通过 ELISA 和免疫荧光染色测量黑素细胞的 DNA 损伤、环丁烷嘧啶二聚体(CPD)和细胞增殖标志物 Ki-67。通过流式细胞术和 PCR 阵列及 RT-qPCR 评估细胞凋亡。

结果

正常人体表皮黑素细胞在承受 UVB 辐射后仍能存活和增殖,同时产生 DNA 损伤。皮肤共生菌表皮葡萄球菌及其产物 LTA 通过上调 TRAF1、CASP14、CASP5 和 TP73 促进黑素细胞的存活。另一方面,痤疮丙酸杆菌可通过增加凋亡来抑制 UVB 照射的黑素细胞存活。

结论

我们的研究显示了在照射过程中共生菌对黑素细胞的不同作用方面。不同皮肤共生菌之间可能达到的平衡会影响 NHM 成为癌细胞的潜力。

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