PMID- 24980870
OWN - NLM
STAT- MEDLINE
DCOM- 20141229
LR  - 20140906
IS  - 1872-9142 (Electronic)
IS  - 0161-5890 (Linking)
VI  - 62
IP  - 1
DP  - 2014 Nov
TI  - IgE in the absence of allergen induces the expression of monocyte chemoattractant 
      protein-1 in the rat basophilic cell-line RBL-2H3.
PG  - 114-21
LID - S0161-5890(14)00139-4 [pii]
LID - 10.1016/j.molimm.2014.06.008 [doi]
AB  - 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.
CI  - Copyright (c) 2014 Elsevier Ltd. All rights reserved.
FAU - Ahn, Ki Bum
AU  - Ahn KB
AD  - Department of Oral Microbiology and Immunology, DRI, and BK21 Plus Program, 
      School of Dentistry, Seoul National University, 28 Yongon-Dong, Chongno-Gu, Seoul 
      110-749, Republic of Korea.
FAU - Jeon, Jun Ho
AU  - Jeon JH
AD  - Division of High-risk Pathogen Research, Center for Infectious Diseases, Korean 
      National Institute of Health, Cheongwon-gun, Chungbuk 363-951, Republic of Korea.
FAU - Kang, Seok-Seong
AU  - Kang SS
AD  - Department of Oral Microbiology and Immunology, DRI, and BK21 Plus Program, 
      School of Dentistry, Seoul National University, 28 Yongon-Dong, Chongno-Gu, Seoul 
      110-749, Republic of Korea.
FAU - Chung, Dae Kyun
AU  - Chung DK
AD  - School of Biotechnology and Institute of Life Science and Resources, Kyung Hee 
      University, Yongin 446-701, Republic of Korea.
FAU - Yun, Cheol-Heui
AU  - Yun CH
AD  - Department of Agricultural Biotechnology and Research Institute for Agriculture 
      and Life Sciences, Seoul National University, Seoul 151-921, Republic of Korea.
FAU - Han, Seung Hyun
AU  - Han SH
AD  - Department of Oral Microbiology and Immunology, DRI, and BK21 Plus Program, 
      School of Dentistry, Seoul National University, 28 Yongon-Dong, Chongno-Gu, Seoul 
      110-749, Republic of Korea. Electronic address: shhan-mi@snu.ac.kr.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20140628
PL  - England
TA  - Mol Immunol
JT  - Molecular immunology
JID - 7905289
RN  - 0 (Allergens)
RN  - 0 (Ccl2 protein, rat)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Transcription Factor AP-1)
RN  - 37341-29-0 (Immunoglobulin E)
RN  - EC 2.7.11.13 (Protein Kinase C)
SB  - IM
MH  - Allergens/immunology
MH  - Animals
MH  - Basophils/drug effects/*immunology
MH  - Cell Line
MH  - Chemokine CCL2/genetics/*immunology
MH  - Gene Expression/drug effects
MH  - Immunoglobulin E/*immunology
MH  - Inflammation/genetics/immunology/metabolism
MH  - MAP Kinase Signaling System/drug effects
MH  - Protein Kinase C/physiology
MH  - Rats
MH  - Transcription Factor AP-1/genetics/metabolism
MH  - Up-Regulation/drug effects/genetics
OTO - NOTNLM
OT  - Basophils
OT  - Immunoglobulin E
OT  - Monocyte chemoattractant protein-1
EDAT- 2014/07/02 06:00
MHDA- 2014/12/30 06:00
CRDT- 2014/07/02 06:00
PHST- 2014/02/20 00:00 [received]
PHST- 2014/05/28 00:00 [revised]
PHST- 2014/06/08 00:00 [accepted]
PHST- 2014/07/02 06:00 [entrez]
PHST- 2014/07/02 06:00 [pubmed]
PHST- 2014/12/30 06:00 [medline]
AID - S0161-5890(14)00139-4 [pii]
AID - 10.1016/j.molimm.2014.06.008 [doi]
PST - ppublish
SO  - Mol Immunol. 2014 Nov;62(1):114-21. doi: 10.1016/j.molimm.2014.06.008. Epub 2014 
      Jun 28.