Inhibition of mast cell-dependent anaphylaxis by sodium salicylate

Sodium salicylate (NaSal) is a commonly used agent with a wide pharmacological spectrum. The objective of the present study was to investigate the effect of NaSal on anaphylaxis. NaSal (10−1 and 1 mm) significantly inhibited systemic anaphylaxis induced by compound 48/80 in rats. NaSal also significantly inhibited local anaphylaxis activated by anti-dinitrophenyl (DNP) immunoglobulin E (IgE). NaSal (10−1 and 1 mm) significantly inhibited histamine release from rat peritoneal mast cells (RPMC) activated by compound 48/80 or anti-DNP IgE. Northern-blot analysis demonstrated that a significantly reduced level of the mRNA of l-histidine decarboxylase was expressed in mast cells treated with NaSal, compared with that without NaSal. NaSal (10−2 and 10−1 mm) had a significant inhibitory effect on anti-DNP IgE-induced tumour necrosis factor-α secretion from RPMC. The level of cyclic AMP in RPMC, when NaSal (1 mm) was added, transiently and significantly increased about sixfold compared with that of basal cells. These results suggest a possible use of NaSal in managing mast cell-dependent anaphylaxis

Association between SNP rs1800875, serum chymase and immunoglobulin E levels in patients with coronary heart disease*

Objective: The gene for mast cell chymase (CMA1) is an ideal candidate for investigating the genetic predisposition to coronary heart disease (CHD), as activated mast cells have been found to be present in a greater proportion in the shoulder region of atheroma than in normal coronary intimae. Previous studies have indicated that CMA1 promoter polymorphism rs1800875 may be involved in regulating immunoglobulin E (IgE) levels in patients with eczema, and it is associated with the progression of immunoglobulin A nephropathy. Methods: The association between single nucleotide polymorphism (SNP) rs1800875, serum chymase, and serum IgE levels was examined in 175 CHD subjects and 95 non-CHD subjects. Results: Statistical analysis indicated no significant difference in allele frequency between CHD and non-CHD. However, a significant association was found between CMA1 genotypes and total IgE levels in CHD subjects. Meanwhile, crossover analysis revealed that, in GG homozygotes, CHD risk was nearly six times higher in those with IgE (U/ml) level <2.58 (natural logarithm conversion), while no association was found with chymase level. Conclusions: Polymorphism rs1800875 of CMA1 may be associated with serum IgE level in CHD subjects, but not with chymase level in both groups. In GG homozygotes, high IgE level is a protective factor against coronary disease