Dermatology Unit, Azienda Unità Sanitaria Locale-IRCCS di Reggio Emilia, 42122 Reggio Emilia, Italy.
Department of Clinical and Experimental Medicine, Section of Dermatology, University of Messina, 98122 Messina, Italy.
Biomolecules. 2023 Jul 10;13(7):1100. doi: 10.3390/biom13071100.
Microbiome dysbiosis and cytokine alternations are key features of atopic dermatitis (AD) and psoriasis (PsO), two of the most prevalent and burdensome pruritic skin conditions worldwide. Interleukin (IL)-33 and IL-31 have been recognized to be major players who act synergistically in the pathogenesis and maintenance of different chronic inflammatory conditions and pruritic skin disorders, including AD and PsO, and their potential role as therapeutic targets is being thoroughly investigated. The bidirectional interplay between dysbiosis and immunological changes has been extensively studied, but there is still debate regarding which of these two factors is the actual causative culprit behind the aetiopathological process that ultimately leads to AD and PsO. We conducted a literature review on the Pubmed database assessing articles of immunology, dermatology, microbiology and allergology with the aim to strengthen the hypothesis that dysbiosis is at the origin of the IL-33/IL-31 dysregulation that contributes to the pathogenesis of AD and PsO. Finally, we discussed the therapeutic options currently in development for the treatment of these skin conditions targeting IL-31, IL-33 and/or the microbiome.
肠道菌群失调和细胞因子改变是特应性皮炎（AD）和银屑病（PsO）的主要特征，这两种疾病是全球最常见且负担最重的瘙痒性皮肤病。白细胞介素（IL）-33 和 IL-31 已被认为是主要的参与者，它们在不同的慢性炎症性疾病和瘙痒性皮肤病的发病机制和维持中协同作用，包括 AD 和 PsO，它们作为治疗靶点的潜力正在被深入研究。肠道菌群失调和免疫变化之间的双向相互作用已经得到了广泛的研究，但关于这两个因素中哪一个是导致 AD 和 PsO 发病的实际致病因素，仍存在争议。我们在 Pubmed 数据库上进行了文献回顾，评估了免疫学、皮肤病学、微生物学和变态反应学的文章，旨在加强以下假设，即肠道菌群失调是导致 IL-33/IL-31 失调的根源，从而导致 AD 和 PsO 的发病。最后，我们讨论了目前针对这些皮肤疾病的治疗选择，这些治疗选择针对的是 IL-31、IL-33 和/或微生物组。
