concanavalin-a and azelastine

The influence of anti-allergic drugs on lymphocyte function was investigated by examining the blastic activity and cytokine production of human peripheral blood leukocytes in response to concanavalin A stimulation in vitro. Addition of ketotifen, disodium cromoglycate and oxatomide did not influence peripheral blood leukocyte blastic activity even when high concentrations (10.0 micrograms/ml) of these drugs were added to cell cultures. However, azelastine and terfenadine caused inhibition of peripheral blood leukocyte activation. Interleukin-2, interleukin-3, interleukin-4 and interleukin-5 production from peripheral blood leukocytes was strongly suppressed when the cells were cultured in the presence of these agents. This suppression was observed even when lower concentrations (1.0 and 0.5 micrograms/ml) of these agents were added to the cultures.

Topics: Cells, Cultured; Concanavalin A; Cromolyn Sodium; Cytokines; Enzyme-Linked Immunosorbent Assay; Histamine H1 Antagonists; Humans; Interleukin-2; Interleukin-3; Interleukin-4; Interleukin-5; Ketotifen; Lymphocyte Activation; Phthalazines; Piperazines; T-Lymphocytes

Effects of azelastine (AZ) on human peripheral blood leukocytes (PBL) in culture were examined. Addition of 10.0 micrograms/ml of AZ resulted in a marked inhibition of PBL blastic activity, but lower concentrations (1.0 and 0.5 microgram/ml) had no demonstrable suppressive effects on the activation. Interleukin (IL)-2, IL-3 and IL-4 production from PBL in response to Concanavalin A stimulation was also strongly suppressed when the cells were cultured in the presence of AZ. This suppression was observed even when lower concentrations (1.0 and 0.5 microgram/ml) of AZ were added to cell cultures.

Topics: Adult; Cells, Cultured; Concanavalin A; Cytokines; Female; Humans; Leukocytes; Lymphocyte Activation; Male; Middle Aged; Phthalazines

The ability of azelastine and selected antiallergic drugs to inhibit compound 48/80-induced and PS-potentiated, Con A-induced histamine release from RPMC was investigated. Azelastine, ketotifen, theophylline, and DSCG added simultaneously with the secretagogues or preincubated with the RPMC for 10 min before the addition of secretagogues produced concentration-dependent inhibition of histamine release. In general, the relative order of potency at calculated IC50 level was as follows: azelastine greater than ketotifen greater than theophylline greater than DSCG. The preincubation of RPMC with azelastine for 10 min exerted 3.5 times greater inhibition of Con A plus PS-stimulated histamine release but did not influence the inhibitory activity on compound 48/80-induced release. The duration of preincubation did not influence the inhibitory effects of ketotifen with either secretagogue. Theophylline and DSCG exerted significantly greater inhibition when they were added simultaneously with Con A plus PS. The inhibitory activity of DSCG was also significantly improved upon simultaneous addition with compound 48/80. These data demonstrated that azelastine is the most potent inhibitor of nonallergic histamine release from RPMC among the four antiallergic drugs examined.

Topics: Animals; Concanavalin A; Histamine H1 Antagonists; Histamine Release; Male; Mast Cells; p-Methoxy-N-methylphenethylamine; Phosphatidylserines; Phthalazines; Pyridazines; Rats; Rats, Inbred Strains