Pachauri Arun, Sharma Shweta
Parul Institute of Pharmacy, Vadodara, Gujarat, India.
Inflammopharmacology. 2025 Jun 12. doi: 10.1007/s10787-025-01813-y.
Psoriasis is a chronic, multifactorial, inflammatory skin disease, increasingly recognized as a systemic disorder influenced by the gut-skin axis, which is a dynamic bidirectional communication between intestinal microbiome and cutaneous immune response. This narrative review explores the understanding of the gut-skin axis with the latest evidence on how gut dysbiosis occurs in psoriasis, characterized by reduced microbial diversity and its shifts, and how it contributes to pathogenesis and exacerbation of psoriasis. Notably, recent scientific literature evidence suggests that the alteration of gut microbiome in psoriasis includes a decreased level of beneficial species like Faecalibacterium prausnitzii and a rise in the level of proinflammatory bacterial species like Prevotella copri. Mechanistic insights reveal that gut-derived metabolites, impaired barrier functions, and immune signaling, particularly involving IL-23 and Th17 cells, play a pivotal role in this axis, linking intestinal health to cutaneous manifestations. Both animal and human trials underscore the therapeutic potential of interventions targeting the gut microbiota, including prebiotics, probiotics, dietary modifications, and FMT, demonstrating some promising but variable effects on disease severity and systemic inflammation. Despite these advances, translating the gut-skin axis into clinical practice presents a notable challenge due to limited scientific evidence, a lack of standardised microbiome profiling, and the absence of universally accepted biomarkers to monitor and stratify therapeutic outcomes. These limitations hinder the development of personalised care approaches and the integration of the gut-skin axis as a promising frontier in many autoimmune diseases, where the gut-skin axis and the intestinal microbiome play a crucial role.
银屑病是一种慢性、多因素的炎症性皮肤病,越来越被认为是一种受肠-皮肤轴影响的系统性疾病,肠-皮肤轴是肠道微生物群与皮肤免疫反应之间动态的双向交流。本叙述性综述探讨了对肠-皮肤轴的理解,以及关于银屑病中肠道菌群失调如何发生的最新证据,其特征为微生物多样性降低及其变化,以及它如何导致银屑病的发病机制和病情加重。值得注意的是,最近的科学文献证据表明,银屑病中肠道微生物群的改变包括有益菌如普拉梭菌水平的降低和促炎菌如柯氏普雷沃菌水平的升高。机制研究表明,肠道衍生的代谢产物、受损的屏障功能和免疫信号传导,特别是涉及白细胞介素-23和辅助性T细胞17,在这个轴中起关键作用,将肠道健康与皮肤表现联系起来。动物试验和人体试验都强调了针对肠道微生物群的干预措施的治疗潜力,包括益生元、益生菌、饮食调整和粪菌移植,这些措施对疾病严重程度和全身炎症表现出一些有前景但效果不一的影响。尽管有这些进展,但由于科学证据有限、缺乏标准化的微生物群分析以及缺乏普遍接受用于监测和分层治疗结果的生物标志物,将肠-皮肤轴转化为临床实践面临着显著挑战。这些限制阻碍了个性化护理方法的发展以及肠-皮肤轴作为许多自身免疫性疾病中有前景的前沿领域的整合,在这些疾病中肠-皮肤轴和肠道微生物群起着关键作用。