Imidacloprid inhibits IgE-mediated RBL-2H3 cell degranulation and passive cutaneous anaphylaxis
10.5415/apallergy.2016.6.4.236
- Author:
Linbo SHI
1
;
Li ZOU
;
Jinyan GAO
;
Huaing XU
;
Xiaoyun SHI
;
Hongbing CHEN
Author Information
1. State Key Laboratory of Food Science and Technology, Nanchang University, Nanchang 330047, China. chenhongbing@ncu.edu.cn
- Publication Type:Original Article
- Keywords:
Imidacloprid;
Mast cells;
Ca²⁺ influx
- MeSH:
Animals;
Basophils;
Cell Degranulation;
Cell Line;
Crop Protection;
Histamine;
Hypersensitivity;
Interleukin-6;
Leukemia;
Leukotriene C4;
Mast Cells;
Necrosis;
Passive Cutaneous Anaphylaxis;
Rats;
Receptors, Nicotinic
- From:
Asia Pacific Allergy
2016;6(4):236-244
- CountryRepublic of Korea
- Language:English
-
Abstract:
BACKGROUND: Imidacloprid has been commonly used as a pesticide for crop protection and acts as nicotinic acetylcholine receptor agonists. Little information about the relationship between imidacloprid and allergy is available. OBJECTIVE: This study aims to examine the effects of imidacoprid on IgE-mediated mast cell activation. METHODS: The rat basophilic leukemia cell line RBL-2H3 (RBL-2H3 cells) were treated with 10⁻³ – 10⁻¹² mol/L imidacloprid, followed by measuring the mediator production, influx of Ca²⁺ in IgE-activated RBL-2H3 cells, and the possible effects of imidacoprid on anti-dinitrophenyl IgE-induced passive cutaneous anaphylaxis (PCA). RESULTS: It was shown that imidacoprid suppressed the production of histamine, β-hexosaminidase, leukotriene C4, interleukin-6, tumor necrosis factor-α, and Ca²⁺ mobilization in IgE-activated RBL-2H3 cells and decreased vascular extravasation in IgE-induced PCA. CONCLUSION: It is the first time to show that imidacloprid suppressed the activation of RBL-2H3 cells.
