Chitinase 3-like 1 is involved in the induction of IL-8 expression by double-stranded RNA in airway epithelial cells

被引:8
作者
Lee, Jae Woo [1 ]
Kim, Mi Na [1 ]
Kim, Eun Gyul [1 ]
Leem, Ji Su [1 ]
Baek, Seung Min [1 ]
Kim, Min Jung [2 ]
Kim, Kyung Won [1 ]
Sohn, Myung Hyun [1 ]
机构
[1] Yonsei Univ, Coll Med, Brain Korea 21 Project, Dept Pediat,Severance Hosp,Inst Allergy, 134 Sinchon Dong, Seoul 03722, South Korea
[2] Yonsei Univ, Yongin Severance Hosp, Dept Pediat, 363 Dongbaekjukjeon Daero, Yongin 16995, Gyeonggi Do, South Korea
基金
新加坡国家研究基金会;
关键词
Airway epithelial cell; Chitinase; 3-like; 1; Interleukin-8; MAPK signaling Pathway; Respiratory syncytial virus; TOLL-LIKE RECEPTOR-3; INFLAMMATION; PATHWAYS; PROTEIN; LUNG; PROLIFERATION; INTERLEUKIN-8; RESPONSES; ASTHMA; MAPK;
D O I
10.1016/j.bbrc.2022.01.008
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Viral respiratory infection causes inflammatory lung disease. Chitinase 3-like 1 (CHI3L1) contributes to airway inflammation, but its role in human airway epithelial cells following viral infection is unclear. Thus, we investigated whether CHI3L1 regulates inflammatory responses caused by viral infections in airway epithelial cells. Human bronchial epithelial cells, BEAS-2B, were stimulated with a synthetic analog of viral double-stranded RNA, polyinosinic:polycytidylic acid (poly(I:C)). To confirm the specific role of CHI3L1, CHI3L1 was knocked down in BEAS-2B cells using shRNA lentivirus. The expression of CHI3L1 and proinflammatory cytokines such as IL-8 and phosphorylation of mitogen-activated protein kinase (MAPK) pathways were analyzed. In addition to poly(I:C), BEAS-2B cells were infected with the human respiratory syncytial virus (RSV) A2 strain, and CHI3L1 and IL-8 expression was analyzed. Stimulating the cells with poly(I:C) increased CHI3L1 and IL-8 expression, whereas IL-8 expression was abrogated in CHI3L1 knockdown BEAS-2B cells. Poly(I:C) stimulation of BEAS-2B cells resulted in phosphorylation of MAPK pathways, and inhibition of MAPK pathways significantly abolished IL-8 secretion. Phosphorylation of MAPK pathways was diminished in CHI3L1 knockdown BEAS-2B cells. Infection with RSV increased CHI3L1 and IL-8 expression. IL-8 expression induced by RSV infection was abrogated in CHI3L1 knockdown cells. In conclusion, CHI3L1 may be involved in IL-8 secretion by regulating MAPK pathways during respiratory viral infections in airway epithelial cells. (c) 2022 Elsevier Inc. All rights reserved.
引用
收藏
页码:106 / 112
页数:7
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