Polyinosinic-polycytidylic acid induces the expression of GRO-α in BEAS-2B cells

被引：15

作者：

Yamashita, K

Imaizumi, T

Taima, K

Fujita, T

Ishikawa, A

Yoshida, H

Oyama, C

Satoh, K

机构：

[1] Hirosaki Univ, Sch Med, Dept Vasc Biol, Inst Brain Sci, Hirosaki, Aomori 0368562, Japan

[2] Hirosaki Univ, Sch Med, Dept Internal Med 2, Hirosaki, Aomori 0368562, Japan

[3] Tokyo Metropolitan Inst Med Sci, Dept Tumor Biol, Tokyo 113, Japan

[4] Hirosaki Univ, Sch Med, Dept Urol, Hirosaki, Aomori 0368562, Japan

来源：

INFLAMMATION | 2005年 / 29卷 / 01期

关键词：

poly IC; bronchial epithelial cells; GRO-alpha; dsRNA; IRF-3; RIG-I;

D O I：

10.1007/s10753-006-8964-4

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Growth-related oncogene protein-alpha (GRO-alpha)/CXCLl is a chemokine that activates neutrophils and plays an important role in inflammatory reactions. Polyinosinic-polycytidylic acid (poly IC) is a synthetic double-stranded RNA (dsRNA), which is a ligand for Toll-like receptor-3. Poly IC mimics viral infection when applied to cells and induces inflammatory and immune responses. In the present study, we found the induction of GRO-alpha in BEAS-2B bronchial epithelial cells treated with poly IC. Pretreatment of cells with 2-aminopurine, an inhibitor for dsRNA-dependent protein kinase (PKR), inhibited the expression of GRO-alpha-induced by poly IC. Overexpression of interferon-regulatory factor-3 (IRF-3) or retinoic-acid inducible gene-I (RIG-I) enhanced the induction of GRO-alpha by poly IC. PKR, IRF-3, and RIG-I may be involved in the poly IC-induced expression of GRO-alpha in BEAS-2B cells. Airway viral infection may elicit GRO-alpha expression in the bronchial epithelium, which may be implicated in inflammatory and immune reactions.

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页码：17 / 21

页数：5

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