寻常痤疮中微生物生态失调和痤疮表皮杆菌CAMP因子相互作用的见解。

IF 4 2区 生物学 Q1 GENETICS & HEREDITY
Qi Chen, Congyu Liu, Juan Tao, Weihong Zeng, Zhongliang Zhu, Chengbing Yao, Yuhua Shang, Jun Tang, Tengchuan Jin
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引用次数: 0

摘要

寻常性痤疮是一种常见的皮肤状况,其特征是形成粉刺,丘疹,脓疱和结节,其根本原因尚未完全了解。本研究探讨了微生物生态失调和毒力因素对痤疮发展的影响。通过高通量16S rRNA测序,我们发现了皮肤微生物组的显著破坏,特别是在粉刺中。使用体外和体内模型评估痤疮表皮杆菌的关键毒力因子,即克里斯蒂-阿特金斯-蒙克-彼得森(CAMP)因子。其中,CAMP2和CAMP5在角化细胞中表现出最高的炎症和溶血活性。在小鼠模型中局部抗il -8治疗可有效减轻炎症并抑制CAMP表达。CAMP3的结构分析揭示了不同的致病特征,这些特征与CAMP5一起加重了痤疮样炎症和皮脂腺萎缩。这些发现促进了我们对微生物生态失调和CAMP因子在痤疮发病机制中的相互作用的理解,为治疗干预提供了潜在的途径。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Insights into microbial dysbiosis and Cutibacterium acnes CAMP factor interactions in acne vulgaris.

Acne vulgaris is a common skin condition marked by the formation of comedones, papules, pustules and nodules, with its underlying causes still not fully understood. This study explores the impact of microbial dysbiosis and virulence factors on acne development. Through high-throughput 16S rRNA sequencing, we identified significant disruptions in the skin microbiome, particularly in comedones. Key virulence factors of Cutibacterium acnes, known as Christie-Atkins-Munch-Peterson (CAMP) factors, were assessed using both in vitro and in vivo models. Among these, CAMP2 and CAMP5 demonstrated the highest inflammatory and haemolytic activities in keratinocytes. Topical anti-IL-8 treatment in a murine model effectively reduced inflammation and suppressed CAMP expression. Structural analysis of CAMP3 uncovered distinct pathogenic features that, alongside CAMP5, were found to aggravate acne-like inflammation and sebaceous gland atrophy. These findings advance our understanding of the interplay between microbial dysbiosis and CAMP factors in acne pathogenesis, offering potential avenues for therapeutic intervention.

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来源期刊
Microbial Genomics
Microbial Genomics Medicine-Epidemiology
CiteScore
6.60
自引率
2.60%
发文量
153
审稿时长
12 weeks
期刊介绍: Microbial Genomics (MGen) is a fully open access, mandatory open data and peer-reviewed journal publishing high-profile original research on archaea, bacteria, microbial eukaryotes and viruses.
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