ABSTRACT
Objective:To explore the key genes and pathways that may play an important role in the pathogenesis of acne by bioinformatics analysis.Methods:GSE6475 and GSE53795 datasets were collected from GEO database, and 18 acne lesions tissues and 18 normal skin tissues were compared. David database was used to analyze the gene ontology (GO) and the key pathway (Kyoto Encyclopedia of genes and genomes, KEGG) of the differential genes, to establish the protein interaction network of the differential genes, and to obtain the most relevant key genes and important clusters.Results:A total of 314 up-regulated genes and 62 down-regulated genes were filtered from those GEO profiles. KEGG pathway analysis showed that these differential genes were mainly enriched in Staphylococcus aureus infection, osteoclast differentiation, pentose and glucuronate interconversions. In addition, 379 nodes and ten key genes (CXCL8, PTPRC, IL1B, ITGB2, CXCR4, ICAM1, CCR5, SELL, C3AR1 and PLEK) were screened out by protein interaction network.Conclusions:The key genes and pathways identified in this study may be new targets for intervention in the development of acne.
ABSTRACT
Objective To evaluate effects of interleukin-36α (IL-36α) on psoriasiform skin lesions and C-C motif chemokine ligand 20 (CCL20) expression in mice.Methods Totally,30 BALB/c female mice were randomly and equally divided into 3 groups:control group treated with topical vaseline cream on the shaved back and intracutaneous injection with phosphate buffer saline (PBS),model group treated with topical imiquimod cream on the shaved back and intracutaneous injection with PBS,experimental group treated with topical imiquimod cream on the shaved back and intracutaneous injection with IL-36α solution.Psoriasis area severity index (PASI) was used to evaluate changes of psoriasiform skin lesions in mice,and light microscopy to observe morphological changes of skin lesions and to measure the thickness of the epidermis.Real-time fluorescence-based quantitative PCR (qRT-PCR) and Western blot analysis were performed to determine the expression of IL-36α in skin lesions in the control group and model group,and qRT-PCR,Western blot analysis and immunohistochemical study to evaluate changes of CCL20 levels in skin lesions.Results The model group showed significantly increased mRNA (△ Ct value:0.0195 ± 0.0059) and protein expression (3.922 ± 0.248) of IL-36α compared with the control group (mRNA:0.0012 ± 0.0004,P ＜ 0.05;protein:0.690 ± 0.025,P ＜ 0.05).The mRNA and protein expression of CCL20 were significantly higher in the experimental group than those in the model group (mRNA:2.152 ± 0.793 vs.0.999 ± 0.178;protein:0.397 ± 0.033 vs.0.145 ± 0.030;both P ＜ 0.05),and higher in the model group than those in the control group (mRNA:0.378 ± 0.075;protein:0.025 ± 0.009;both P ＜ 0.05).Immunohistochemical study showed that the expression intensity of CCL20 in skin lesions significantly increased in the experimental group compared with that in the model group (Z =2.294,P ＜ 0.05).Conclusion IL-36α may aggravate psoriasiform skin inflammation in mice by promoting CCL20 expression.