蛋白酵素
蛋白酶
舍宾
蛋白酶抑制剂(药理学)
丝氨酸蛋白酶
生物
免疫学
呼吸上皮
卵清蛋白
屋尘螨
细胞因子
刺激
过敏原
上皮
免疫系统
过敏
酶
生物化学
内分泌学
病毒
基因
病毒载量
遗传学
抗逆转录病毒疗法
作者
Çağatay Karaaslan,Dilara Karaguzel,Basak Ezgi Sarac,Ceren Sucularlı,Hayriye Akel Bilgiç,Ömer Kalaycı
出处
期刊:International Archives of Allergy and Immunology
[S. Karger AG]
日期:2021-08-20
卷期号:183 (1): 25-33
被引量:3
摘要
Airway epithelial cells are constantly exposed to intracellular and extracellular proteases that play a pivotal role in several airway diseases. Dermatophagoides pteronyssinus (Der p) 1 derived from house dust mite has protease activity that causes epithelial barrier defect and inflammatory response. Protease inhibitors released against proteases are involved in the maintenance of homeostasis. A disruption of the balance between proteases and protease inhibitors can lead to distortion of the cellular structures and cellular activities and thus culminate in disease processes. Although the effects of Der p 1 allergen on epithelial barrier integrity and inflammatory response are well-established, its contribution to protease inhibitor production is highly limited.This study aimed to determine the profile of the protease inhibitor response to Der p 1 allergen in human airway epithelial cells, A549 and BEAS-2B.Differentiated cells by the air-liquid interface were exposed to Der p 1 with or without Th2 type cytokines (IL-4 and IL-13). Gene expression of protease inhibitors was determined by qPCR at 2 different time points.We found that the effect of allergen exposure on the protease inhibitor profile can vary depending on the antigen concentration, treatment duration, and the presence or absence of type 2 cytokines. Gene expressions of serine protease inhibitor (SERPIN)B3 and SERPINB4 were increased following Th2 cytokine stimulation in both cell types at both time points, whereas SERPINB2 and TFPI-2 expressions were induced by 24-h Der p 1 stimulation in both cells.Our study suggests that Der p 1 exposure of the airway epithelium may have consequences related to its protease activity in the presence as well as in the absence of Th2 cytokines in the microenvironment.
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