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.