Yibing Zeng

and 3 more

Background: As a polyphenolic compound originated from the food spice turmeric, curcumin (CUR) has various pharmacological effects, such as anti-inflammatory, anti-oxidation, anti-proliferative and anti-angiogenic activities. Psoriasis is centered on the overproduction of Th1- and Th2-related cytokines (e. g. IL-23, IL-17, TNF-α, IL-22), which is involved in the occurrence and development of its pathogenesis. However, whether CUR is involved in the treatment of psoriasis and its specific mechanisms are not fully understood. Methods: In this study, we detected the therapeutic effect of CUR (100mg/kg· d) on IMQ-induced dermatitis in mice, analyzed by PASI scores, ELISA, HE staining, immunofluorescence. Moreover, we further confirmed the alteration in the relative abundance of the gut microbiota through 16sRNA to explore whether CUR could regulate the gut microbiota of IMQ-induced mice. Result: Through intragastric administration, CUR can alleviate psoriasis-like lesions of mice by decreasing PASI scores, reducing the level of IL-6, IL-17A, IL-22, IL-23, TNF-α and TGF-β1, promoting the expression of IL-10. Moreover, 16 sRNA sequencing revealed that CUR could regulate the alteration in the abundance alteration of gut microbiota related to inflammation, such as Alistipes, Mucispirillum and Rikenella at genus level. The correlation analysis further confirmed the close association between important microflora and psoriasis-like inflammation indicators. Conclusions: CUR exerts the effect of alleviating dermatitis of psoriatic mice by regulating Th-17 related inflammatory factors. Moreover, the changes in gut microbiota via CUR may be another factor of relieving IMQ-induced lesions in mice. Therefore, CUR may be a highly promising candidate for the treatment of psoriasis.

Zhuohang Liu

and 4 more

Background: Psoriasis is a recurrent chronic skin inflammatory disease. Its biomarkers are currently inaccurate and lack specificity. Hence, the immune infiltration mechanism of the key differential genes in psoriasis and related principles are discussed in this article. Methods: The GSE30999, GSE67853 and GSE78097 data sets were downloaded from the Gene Expression Omnibus(GEO) database, and the differentially expressed genes were screened with p<0.05 & |Log2FC|>1 by R language. Then, hub genes were picked out through LASSO and BORUTA analyses and verified in exterior dataset GSE83582. Further, we used ssGSEA to evaluate the effect of genes on immune infiltration. GSVA and GSEA algorithms were applied to assess associations between hub genes and different pathways for enrichment. Finally, the gene selection model of psoriasis-based immune infiltration will be examined by ROC. Results: The characteristic genes of psoriasis are determined to be TMPRSS11D, S100A12 and KYNU by the intersection of two algorithms. These three genes all have strong correlations with the content of immune cells and immune-related genes. Highly expressed TMPRSS11D, S100A12, and KYNU genes are involved in HEME_METABOLISM, XENOBIOTIC_METABOLISM, and MTORC1 pathways indicating that core genes affect the development and progression of psoriasis by regulating metabolism and T cell-related immunity. GESA showed that hub genes are linked to immune factors concerning enriched pathways. The AUC values of these three core genes are TMPRSS11D = AUC: 0.980 (0.959–1.000), S100A12= AUC: 0.982 (0.963–1.000), KYNU= AUC: 0.992 (0.982–1.000). Hub genes are actively associated with each other. Eventually, the differential gene expression of these key genes is validated by external datasets. Conclusion: Combining bioinformatics to analyze the immune infiltration mechanism of psoriasis provides a basis for discovering novel diagnostic biomarkers.