IgE in the absence of allergen induces the expression of monocyte chemoattractant protein-1 in the rat basophilic cell-line RBL-2H3

被引:12
作者
Ahn, Ki Bum [1 ,2 ]
Jeon, Jun Ho [3 ]
Kang, Seok-Seong [1 ,2 ]
Chung, Dae Kyun [4 ,5 ]
Yun, Cheol-Heui [6 ,7 ]
Han, Seung Hyun [1 ,2 ]
机构
[1] Seoul Natl Univ, Sch Dent, Dept Oral Microbiol & Immunol, DRI, 28 Yongon Dong, Seoul 110749, South Korea
[2] Seoul Natl Univ, Sch Dent, BK21 Plus Program, Seoul 110749, South Korea
[3] Korean Natl Inst Hlth, Ctr Infect Dis, Div Highrisk Pathogen Res, Chungbuk 363951, South Korea
[4] Kyung Hee Univ, Sch Biotechnol, Yongin 446701, South Korea
[5] Kyung Hee Univ, Inst Life Sci & Resources, Yongin 446701, South Korea
[6] Seoul Natl Univ, Dept Agr Biotechnol, Seoul 151921, South Korea
[7] Seoul Natl Univ, Res Inst Agr & Life Sci, Seoul 151921, South Korea
基金
新加坡国家研究基金会;
关键词
Immunoglobulin E; Monocyte chemoattractant protein-1; Basophils; FC EPSILON RI; NF-KAPPA-B; MAST-CELLS; CYTOKINE PRODUCTION; SIGNALING PATHWAYS; MIP-1; ALPHA; KINASE JNK; MCP-1; ACTIVATION; CHEMOKINES;
D O I
10.1016/j.molimm.2014.06.008
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
070307 [化学生物学]; 071010 [生物化学与分子生物学];
摘要
Recently, basophils have been suggested to produce inflammatory mediators in response to IgE in the absence of allergens. Monocyte chemoattractant protein-1 (MCP-1) plays an important role in the initiation of inflammatory responses by recruiting various immune cells to the site of allergic inflammation. In the present study, we examined whether IgE under allergen-free conditions could stimulate basophils and lead to the production of MCP-1. Exposure of the rat basophilic cell-line RBL-2H3 to IgE without allergen resulted in a dose- and time-dependent induction of MCP-1 expression at both the mRNA and protein level. Although allergen was not necessary for IgE-induced MCP-1 expression, it was essential for degranulation as determined by beta-hexosaminidase release assay. IgE enhanced phosphorylation of MAP kinases including ERK, p38 kinase, and JNK. However, IgE-induced MCP-1 expression was attenuated by inhibitors for JNK and PKC. Concomitantly, IgE induced activation of AP-1, which is an important transcription factor for MCP-1 gene expression in RBL-2H3 cells. Taken together, our results suggest that IgE alone is sufficient to stimulate basophils to increase expression of MCP-1, which in turn might contribute to the inflammatory response. (C) 2014 Elsevier Ltd. All rights reserved.
引用
收藏
页码:114 / 121
页数:8
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