中华皮肤科杂志 ›› 2008, Vol. 41 ›› Issue (10): 674-676.

• 论著 • 上一篇    下一篇

幽门螺杆菌致BALB/c小鼠胃黏膜肥大细胞脱颗粒及黏膜通透性的变化

吕静 李惠 周汛 蔡涛   

  1. 重庆医科大学附属第一医院皮肤性病科 重庆医科大学附属第一医院皮肤科 重庆医科大学附属第一医院皮肤科
  • 收稿日期:2007-12-13 修回日期:2008-03-03 发布日期:2008-10-15
  • 通讯作者: 李惠 E-mail:Lihui131128@vip.163.com

Helicobacter pylori induces changes in the degranulation of mast cells and the permeability of gastric mucosa in BALB/c mice

  

  • Received:2007-12-13 Revised:2008-03-03 Published:2008-10-15

摘要: 目的 探讨幽门螺杆菌(Hp)对小鼠胃黏膜内肥大细胞(MC)脱颗粒及对胃黏膜通透性的影响,以佐证Hp在慢性荨麻疹(CU)发病机制中的作用。方法 70只健康BALB/c小鼠随机分成3组。Hp组30只,每间隔3日灌喂1次Hp菌液,共7次;对照组两组,各20只,分别灌喂45%的乙醇和2%的牛血清白蛋白(BSA)。以蔗糖浓度的变化作为胃黏膜通透性变化的标志,并用甲苯胺蓝染色法(TB)观察灌胃后小鼠胃黏膜内MC总数、脱颗粒MC总数以及脱颗粒MC的百分比。结果 三组小鼠胃黏膜MC总数间的差异有统计学意义(F = 207.59,P < 0.01);且脱颗粒MC百分比之间的差异也有统计学意义(F = 108.16,P < 0.01),Hp组最多,乙醇组次之。Hp组、乙醇组小鼠灌胃后其外周血中的蔗糖浓度较灌胃前明显增加,且乙醇组高于Hp组; BAS组小鼠灌胃前后其外周血中的蔗糖浓度无明显变化(F = -4.06,P > 0.01),与Hp组和乙醇组比较差异有统计学意义(F = 277.03,P < 0.01)。结论 Hp感染可导致小鼠胃黏膜MC数量增加,脱颗粒增多,从而释放组胺和一系列血管活性介质到外周血,可能与荨麻疹的表现有关。

关键词: 幽门螺杆菌, 慢性荨麻疹, 肥大细胞, 胃粘膜, 通透性

Abstract: Objective To investigate the effect of Helicobacter pylori (Hp) on the degranulation of mast cells and the permeability of gastric mucosa in BALB/c mice, in order to provide further evidence for the important role of Hp in the pathogenesis of chronic urticaria (CU). Methods Seventy healthy BALB/c mice were randomly classified into 3 different groups, namely, Hp group (n = 30), fed with Hp liquid once every 3 days for a total of 7 times, and two control groups, alcohol group (n = 20) fed with 45 percent alcohol solution, and bovine serum albumin (BSA) group (n = 20) fed with BSA 2% solution. Alteration in the blood sucrose level was used to assess the permeability of gastric mucosa. Toluidine blue staining of gastric mucosa was used to assess the total number of mast cells, the amount of degranulated mast cells and the percentage of degranulated cells after feeding. Results There was a statistically significant difference between the total number of mast cells (F = 207.59, P < 0.01) and the percentage of degranulated mast cells (F = 108.16, P < 0.01) among the three groups, with the highest number and percentage observed in the Hp group followed by the alcohol group. In both groups, the concentration of blood sucrose was increased after feeding, with a higher increase in the alcohol group; no significant change occurred in the concentration of blood sucrose in the BSA group (F = -4.06, P > 0.05), which differed significantly from the other two groups (F = 277.03, P < 0.01). Conclusions Hp infection could increase the number and degranulation of mast cells in gastric mucosa, resulting in the release of histamines and vasoactive mediators, which may be related to the manifestation of urticaria.

Key words: Helicobacter pylori, chronic urticaria, mast cell, gastric mucosa, permeability.