The α7-nicotinic Acetylcholine Receptors Mediate the Imidacloprid-Induced Inhibition of Mast Cell Degranulation Through Syk Signaling Pathway

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• 英文论文题名：The α7-nicotinic Acetylcholine Receptors Mediate the Imidacloprid-Induced Inhibition of Mast Cell Degranulation Through Syk Signaling Pathway
• 论文作者：Shi Linbo ; Zou Linbo ; Gao Jinyan ; Chen Hongbing
• 英文论文作者：Shi Linbo ; Zou Linbo ; Gao Jinyan ; Chen Hongbing ; State Key Laboratory of Food Science and Technology ; Nanchang University ; School of Food Science ; Nanchang University
• 年：2016
• 作者机构：State Key Laboratory of Food Science and Technology,Nanchang University;School of Food Science,Nanchang University;
• 英文论文关键词：imidacloprid ; α7-nAChR ; mast cell ; Syk signaling pathway
• 会议召开时间：2016-11-04
• 会议录名称：第十一届全国免疫学学术大会摘要汇编
• 英文会议录名称：Abstracts of 2016 CSI Congress on Immunology
• 语种：英文
• 分类号：R593.1
• 学会代码：IGMD
• 会议名称：第十一届全国免疫学学术大会
• 会议地点：中国安徽合肥
• 主办单位：中国免疫学会
• 学会名称：中国免疫学会
• 页数：2
• 文件大小：1336k
• 原文格式：D
• 会议级别：全国

摘要

Backgroud: Imidacloprid has been commonly used as an insecticide for crop protection worldwide and act as nicotinic acetylcholine receptors(nAChRs) agonists. It was shown that nAChRs are involved in the pathology of allergic disease. Among the nicotinic receptors, α7 is the most commonly found nAChR subunit on immune cells.Our previous studies showed that 10-3-10-11 mol /L imidacloprid can inhibit Ig E-mediated mast cell degranulation. However, the underlying mechanism for it remains unclear.Objective: This study aims to further explore the underlying mechanisms by which imidacoprid inhibits the Ig E-meditated mast cell degranulation.Methods:In this study, the Ig E-sensitized rat mast cell/basophil cell line(RBL-2H3) was incubated with methyllycaconitine(MLA),the antagonist of a7-nAChRs, prior to the treatment of imidacloprid, finaly the cells were stimulated with DNP-HAS. Then the allergic mediator production and influx of Ca2+ in Ig E-activated RBL-2H3 and the expression of phosphorylation antibodies in Syk mast cell signaling was measured;Meanwhile, the vascular extravasation in Ig E-induced passive cutaneous anaphylaxis(PCA) of the Balb/c mice ear was investigated.Results:The results showed,compared to the only imidacloprid treatment groups, the groups incubated with MLA, prior to the treatment of imidacloprid have higher amount of histamine, β-hexosaminidase(β-hex), LTC4, IL-6,TNF-α production and Ca2+ influx from Ig E-activated RBL-2H3 and higher phosphorylation content of signaling molecules such as Lyn, Sky, Fyn, ERK, p38, JNK,PLC-γ and NF-κB in mast cell Syk signaling.Furthermore,MLA can also alleviate the inhibition of imidacloprid on Ig E-activated PCA which was induced by mast cell degraunlation.Conclusions:It is the first time to show that the α7-nAChRs mediate the imidacloprid-induced inhibition of mast cell degranulation through Syk signaling pathway.This study suggests that the agonist of α7-nAChR might be a potential therapeutic strategy to control allergic diseases.
Backgroud: Imidacloprid has been commonly used as an insecticide for crop protection worldwide and act as nicotinic acetylcholine receptors(nAChRs) agonists. It was shown that nAChRs are involved in the pathology of allergic disease. Among the nicotinic receptors, α7 is the most commonly found nAChR subunit on immune cells.Our previous studies showed that 10-3-10-11 mol /L imidacloprid can inhibit Ig E-mediated mast cell degranulation. However, the underlying mechanism for it remains unclear.Objective: This study aims to further explore the underlying mechanisms by which imidacoprid inhibits the Ig E-meditated mast cell degranulation.Methods:In this study, the Ig E-sensitized rat mast cell/basophil cell line(RBL-2H3) was incubated with methyllycaconitine(MLA),the antagonist of a7-nAChRs, prior to the treatment of imidacloprid, finaly the cells were stimulated with DNP-HAS. Then the allergic mediator production and influx of Ca2+ in Ig E-activated RBL-2H3 and the expression of phosphorylation antibodies in Syk mast cell signaling was measured;Meanwhile, the vascular extravasation in Ig E-induced passive cutaneous anaphylaxis(PCA) of the Balb/c mice ear was investigated.Results:The results showed,compared to the only imidacloprid treatment groups, the groups incubated with MLA, prior to the treatment of imidacloprid have higher amount of histamine, β-hexosaminidase(β-hex), LTC4, IL-6,TNF-α production and Ca2+ influx from Ig E-activated RBL-2H3 and higher phosphorylation content of signaling molecules such as Lyn, Sky, Fyn, ERK, p38, JNK,PLC-γ and NF-κB in mast cell Syk signaling.Furthermore,MLA can also alleviate the inhibition of imidacloprid on Ig E-activated PCA which was induced by mast cell degraunlation.Conclusions:It is the first time to show that the α7-nAChRs mediate the imidacloprid-induced inhibition of mast cell degranulation through Syk signaling pathway.This study suggests that the agonist of α7-nAChR might be a potential therapeutic strategy to control allergic diseases.

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