Skin Microbiota: Mediator of Interactions Between Metabolic Disorders and Cutaneous Health and Disease.

IF 4.2 2区 生物学 Q2 MICROBIOLOGY Microorganisms Pub Date : 2025-01-14 DOI:10.3390/microorganisms13010161
Magdalini Kreouzi, Nikolaos Theodorakis, Maria Nikolaou, Georgios Feretzakis, Athanasios Anastasiou, Konstantinos Kalodanis, Aikaterini Sakagianni
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Abstract

Metabolic disorders, including type 2 diabetes mellitus (T2DM), obesity, and metabolic syndrome, are systemic conditions that profoundly impact the skin microbiota, a dynamic community of bacteria, fungi, viruses, and mites essential for cutaneous health. Dysbiosis caused by metabolic dysfunction contributes to skin barrier disruption, immune dysregulation, and increased susceptibility to inflammatory skin diseases, including psoriasis, atopic dermatitis, and acne. For instance, hyperglycemia in T2DM leads to the formation of advanced glycation end products (AGEs), which bind to the receptor for AGEs (RAGE) on keratinocytes and immune cells, promoting oxidative stress and inflammation while facilitating Staphylococcus aureus colonization in atopic dermatitis. Similarly, obesity-induced dysregulation of sebaceous lipid composition increases saturated fatty acids, favoring pathogenic strains of Cutibacterium acnes, which produce inflammatory metabolites that exacerbate acne. Advances in metabolomics and microbiome sequencing have unveiled critical biomarkers, such as short-chain fatty acids and microbial signatures, predictive of therapeutic outcomes. For example, elevated butyrate levels in psoriasis have been associated with reduced Th17-mediated inflammation, while the presence of specific Lactobacillus strains has shown potential to modulate immune tolerance in atopic dermatitis. Furthermore, machine learning models are increasingly used to integrate multi-omics data, enabling personalized interventions. Emerging therapies, such as probiotics and postbiotics, aim to restore microbial diversity, while phage therapy selectively targets pathogenic bacteria like Staphylococcus aureus without disrupting beneficial flora. Clinical trials have demonstrated significant reductions in inflammatory lesions and improved quality-of-life metrics in patients receiving these microbiota-targeted treatments. This review synthesizes current evidence on the bidirectional interplay between metabolic disorders and skin microbiota, highlighting therapeutic implications and future directions. By addressing systemic metabolic dysfunction and microbiota-mediated pathways, precision strategies are paving the way for improved patient outcomes in dermatologic care.

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皮肤微生物群:代谢紊乱与皮肤健康和疾病之间相互作用的中介。
代谢紊乱,包括2型糖尿病(T2DM)、肥胖和代谢综合征,是深刻影响皮肤微生物群的全身性疾病,皮肤微生物群是对皮肤健康至关重要的细菌、真菌、病毒和螨虫的动态群落。代谢功能障碍引起的生态失调导致皮肤屏障破坏、免疫失调,并增加对炎性皮肤病的易感性,包括牛皮癣、特应性皮炎和痤疮。例如,T2DM患者的高血糖导致晚期糖基化终产物(AGEs)的形成,AGEs与角化细胞和免疫细胞上的AGEs受体(RAGE)结合,促进氧化应激和炎症,同时促进金黄色葡萄球菌在特应性皮炎中的定植。同样,肥胖引起的皮脂腺脂质组成失调会增加饱和脂肪酸,有利于痤疮角质杆菌的致病菌株,它会产生炎症代谢物,加剧痤疮。代谢组学和微生物组测序的进展揭示了关键的生物标志物,如短链脂肪酸和微生物特征,预测治疗结果。例如,银屑病中丁酸盐水平升高与th17介导的炎症减少有关,而特异性乳杆菌菌株的存在已显示出调节特应性皮炎免疫耐受的潜力。此外,机器学习模型越来越多地用于整合多组学数据,从而实现个性化干预。新兴疗法,如益生菌和后益生菌,旨在恢复微生物多样性,而噬菌体疗法选择性地靶向病原菌,如金黄色葡萄球菌,而不破坏有益菌群。临床试验表明,接受这些针对微生物群的治疗的患者炎症病变显著减少,生活质量指标得到改善。这篇综述综合了代谢紊乱和皮肤微生物群之间双向相互作用的现有证据,强调了治疗意义和未来方向。通过解决全身性代谢功能障碍和微生物群介导的途径,精确的策略为改善皮肤护理患者的结果铺平了道路。
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来源期刊
Microorganisms
Microorganisms Medicine-Microbiology (medical)
CiteScore
7.40
自引率
6.70%
发文量
2168
审稿时长
20.03 days
期刊介绍: Microorganisms (ISSN 2076-2607) is an international, peer-reviewed open access journal which provides an advanced forum for studies related to prokaryotic and eukaryotic microorganisms, viruses and prions. It publishes reviews, research papers and communications. Our aim is to encourage scientists to publish their experimental and theoretical results in as much detail as possible. There is no restriction on the length of the papers. The full experimental details must be provided so that the results can be reproduced. Electronic files and software regarding the full details of the calculation or experimental procedure, if unable to be published in a normal way, can be deposited as supplementary electronic material.
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