Background: Although more and more evidence has supported psoriasis is prone to atherosclerosis, the common mechanism of its occurrence is still not fully elucidated. The purpose of this study is to further explore the molecular mechanism of the occurrence of this complication.Methods: The gene expression profiles of psoriasis (GSE30999) and atherosclerosis (GSE28829) were downloaded from the Gene Expression Omnibus (GEO) database. After identifying the common differentially expressed genes (DEGs) of psoriasis and atherosclerosis, three kinds of analyses were performed, namely functional annotation, protein‐protein interaction (PPI) network and module construction, and hub gene identification and co-expression analysis.Results: A total of 94 common DEGs (24 downregulated genes and 70 upregulated genes) was selected for subsequent analyses. Functional analysis emphasizes the important role of chemokines and cytokines in these two diseases. In addition, lipopolysaccharide-mediated signaling pathway is closely related to both. Finally, 16 important hub genes were identified using cytoHubba, including LYN, CSF2RB, IL1RN, RAC2, CCL5, IRF8, C1QB, MMP9, PLEK, PTPRC, FYB, BCL2A1, LCP2, CD53, NCF2 and TLR2.Conclusions: Our study reveals the common pathogenesis of psoriasis and atherosclerosis. These common pathways and hub genes may provide new ideas for further mechanism research.

Histamine intolerance (HIT) is a common disorder associated with impaired histamine metabolism. Notwithstanding, it is often misdiagnosed as other diseases because of its lack of specific clinical manifestations. HIT did not gain traction until the early 21st century. In this review, we will focus on the latest research and elaborate on the clinical manifestations of HIT, including its manifestations in special populations such as atopic dermatitis (AD) and chronic urticaria (CU), as well as the latest understanding of its etiology and pathogenesis. In addition, we will explore the latest treatment strategies for HIT and the treatment of specific cases.

Aloe vera is a traditional wound‑healing medicine used for the treatment of skin disorders. Aloe polysaccharide (APS) is the main macromolecule of Aloe vera, which contributes to its function. Psoriasis is an immune‑mediated chronic inflammatory disease, which affects 2‑3% of the general population. The conventional remedies used to treat psoriasis demonstrate limited effects; therefore, natural products, including Aloe vera, are being taken into consideration. However, the effects of APS on the treatment of psoriasis and the underlying mechanisms remain to be elucidated. The human keratinocyte cell line HaCaT was used to determine the effects of APS on psoriasis. Cells were randomly divided into five groups: i) Negative control group; ii) tumor necrosis factor (TNF)‑α stimulated psoriasis model group; and iii) APS (20, 40 and 80 µg/ml) pretreated psoriasis groups. Cell viability and proliferation were investigated using the CCK‑8 assay. ELISA and western blotting were applied to study the abundance of interleukin (IL)‑8 and IL‑12 in TNF‑α‑incubated culture medium and APS‑treated HaCaT cells, respectively. In addition, the mRNA expression levels of p65, and the protein expression levels of nuclear factor (NF)‑κB inhibitor‑α (IκBα) and phosphorylated‑p65, were detected by reverse transcription‑quantitative polymerase chain reaction and western blotting, respectively. APS was revealed to significantly reduce TNF‑α‑stimulated elevation of HaCaT cell proliferation in a dose‑dependent manner. The expression levels of inflammatory factors, including IL‑8 and IL‑12, were increased in response to TNF‑α. In addition, the mRNA and protein expression levels of p65 were increased following treatment with TNF‑α. Notably, treatment with APS was demonstrated to significantly attenuate the aforementioned effects in a dose‑dependent manner. Furthermore, IκBα protein expression levels were significantly reduced following treatment with TNF‑α, which was significantly reversed following treatment with APS. In conclusion, these results suggested that APS inhibited TNF‑α‑induced proliferation of keratinocytes and overactivation of the NF‑κB signaling pathway.

Background: Psoriasis is a chronic, prolonged, and recurrent skin inflammatory disease. However, the pathogenesis of psoriasis is not completely clear, thus we aimed to explore potential molecular basis of it.Methods: Two datasets were downloaded from the Gene Expression Omnibus database. After identifying the differentially expressed genes of psoriasis skin lesion samples and healthy controls, three kinds of analyses, namely functional annotation, protein-protein interaction (PPI) network, and immune infiltration analyses, were performed.Results: A total of 152 up-regulated genes and 38 down-regulated genes were selected for subsequent analyses. Evaluation of the PPI network identified the most important module containing 13 hub genes. Gene ontology analysis showed that the hub genes have a significant enrichment effect on positive regulation of cell migration, defense response to the other organism and epithelial cell differentiation. KEGG signaling pathway analysis showed that the hub genes were significantly enriched in chemokine signaling, Toll-like receptor signaling pathway, and IL-17 signaling pathway. Compared with the normal control sample, naive B cells, CD8⁺ T cells, activated memory CD4⁺ T cells, follicular helper T cells, gamma delta T cells, resting NK cells, monocytes, M0 macrophages, M1 macrophages, activated dendritic cells and neutrophils infiltrated more, while memory B cells, naive CD4⁺ T cells, regulatory T cells (Tregs), activated NK cells, resting mast cells, and eosinophils infiltrated less.Conclusion: To conclude, the hub genes and pathways identified from psoriasis lesions and normal controls along with the immune infiltration profile may provide new insights into the study of psoriasis.