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寻常痤疮中微生物群落失调与CAMP因子相互作用的研究进展

Insights into microbial dysbiosis and CAMP factor interactions in acne vulgaris.

作者信息

Chen Qi, Liu Congyu, Tao Juan, Zeng Weihong, Zhu Zhongliang, Yao Chengbing, Shang Yuhua, Tang Jun, Jin Tengchuan

机构信息

Department of Dermatology, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui 230001, PR China.

Laboratory of Structural Immunology, Key Laboratory of Immune Response and Immunotherapy, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui, 230027, PR China.

出版信息

Microb Genom. 2025 Jul;11(7). doi: 10.1099/mgen.0.001449.

Abstract

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 , known as Christie-Atkins-Munch-Peterson (CAMP) factors, were assessed using both and 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.

摘要

寻常痤疮是一种常见的皮肤疾病,其特征为粉刺、丘疹、脓疱和结节的形成,但其根本原因仍未完全明确。本研究探讨了微生物群落失调和毒力因子对痤疮发展的影响。通过高通量16S rRNA测序,我们发现皮肤微生物群存在显著破坏,尤其是在粉刺中。使用[具体模型1]和[具体模型2]模型评估了名为克里斯蒂-阿特金斯-蒙克-彼得森(CAMP)因子的关键毒力因子。其中,CAMP2和CAMP5在角质形成细胞中表现出最高的炎症和溶血活性。在小鼠模型中进行局部抗IL-8治疗可有效减轻炎症并抑制CAMP表达。CAMP3的结构分析揭示了独特的致病特征,发现这些特征与CAMP5一起会加重痤疮样炎症和皮脂腺萎缩。这些发现增进了我们对微生物群落失调与CAMP因子在痤疮发病机制中相互作用的理解,为治疗干预提供了潜在途径。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cb85/12265948/263920e27c49/mgen-11-01449-g001.jpg

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