Objective Psoriasis is an immune-mediated inflammatory *** advances in the study of its pathogenesis,the exact development mechanism of psoriasis remains to be fully *** epidermis plays a crucial role in *** study aim...
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Objective Psoriasis is an immune-mediated inflammatory *** advances in the study of its pathogenesis,the exact development mechanism of psoriasis remains to be fully *** epidermis plays a crucial role in *** study aimed to investigate the effects of interleukin-36β(IL-36β)on keratinocyte dysfunction in *** Human keratinocyte cell lines,HaCaT cells,were treated with 0(control),50 or 100 ng/ml IL-36βrespectively for 24 *** viability was determined with a cell counting kit-8 *** cytometry was used to assess the effects of IL-36βon apoptosis and cell cycle *** of the differentiation markers,such as keratin 10 and involucrin,were evaluated by quantitative real-time polymerase chain reaction(RT-qPCR).Expressions of the inflammatory cytokines,IL-1βand IL-6 were tested by *** CCK8 assay showed the survival rate had no significant difference between the control and treated group(P>0.05).Flow cytometry analysis showed cell cycle arrest at S phase in the IL-36β-treated groups compared with the control group(P<0.05).RT-qPCR verified the decreased mRNA expressions of keratin 10 and involucrin in the IL-36β-treated groups compared with the negative control(P<0.01).ELISA showed 100 ng/ml IL-36βenhanced levels of IL-1βand IL-6 in culture supernatants of HaCaT cells compared with the negative control(P<0.05).Conclusion Taken together,these findings suggest that IL-36βcould induce cell cycle arrest at S phase,inhibit keratin 10 and involucrin expressions and promote inflammatory activity in HaCaT cell lines.
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