IL-36β Promotes Inflammatory Activity and Inhibits Differentiation of Keratinocytes In Vitro  

白细胞介素-36β对体外培养角质形成细胞炎症反应与分化的影响（英文）

作　　者：王文明 吴超 余晓玲 晋红中 

机构地区：[1]中国医学科学院北京协和医学院北京协和医院皮肤科 [2]南方医科大学皮肤病医院皮肤科

出　　处：《Chinese Medical Sciences Journal》2019年第3期199-204,共6页中国医学科学杂志（英文版）

基　　金：Supported by the National Natural Science Foundation of China(No.81773331);CAMS Initiative for Innovative Medicine(No.2017-I2M-B&R-01)

摘　　要：Objective Psoriasis is an immune-mediated inflammatory disease.Despite advances in the study of its pathogenesis,the exact development mechanism of psoriasis remains to be fully elucidated.Hyperproliferative epidermis plays a crucial role in psoriasis.This study aimed to investigate the effects of interleukin-36β(IL-36β)on keratinocyte dysfunction in vitro.Methods Human keratinocyte cell lines,HaCaT cells,were treated with 0(control),50 or 100 ng/ml IL-36βrespectively for 24 h.Cell viability was determined with a cell counting kit-8 assay.Flow cytometry was used to assess the effects of IL-36βon apoptosis and cell cycle distribution.Expressions 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 ELISA.Results 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.Objective Psoriasis is an immune-mediated inflammatory disease. Despite advances in the study of its pathogenesis, the exact development mechanism of psoriasis remains to be fully elucidated. Hyperproliferative epidermis plays a crucial role in psoriasis. This study aimed to investigate the effects of interleukin-36β(IL-36β) on keratinocyte dysfunction in vitro.Methods Human keratinocyte cell lines, HaCaT cells, were treated with 0(control), 50 or 100 ng/ml IL-36β respectively for 24 h. Cell viability was determined with a cell counting kit-8 assay. Flow cytometry was used to assess the effects of IL-36β on apoptosis and cell cycle distribution. Expressions 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-1β and IL-6 were tested by ELISA.Results 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-36β enhanced levels of IL-1β and IL-6 in culture supernatants of HaCaT cells compared with the negative control(P < 0.05). Conclusion Taken together, these findings suggest that IL-36β could induce cell cycle arrest at S phase, inhibit keratin 10 and involucrin expressions and promote inflammatory activity in HaCaT cell lines.

关 键 词：interleukin-36β PSORIASIS KERATINOCYTES INFLAMMATORY activity DIFFERENTIATION 

分 类 号：R73[医药卫生—肿瘤]