Kinins are generated during experimental rhinovirus colds.

We investigated the pathophysiology of rhinovirus colds by challenging volunteers with either of two strains of rhinovirus or with placebo. Nasal lavages were done before challenge and every 4 h for five days after challenge. We measured the levels of histamine, kinins, [3H]-N-alpha-p-tosyl-L-arginine methyl ester (TAME)-esterase activity, and albumin and counted the number of neutrophils in the recovered lavage fluid. Subjects who became both infected and symptomatic showed increases in levels of kinins (P less than .03), TAME-esterase activity (P less than .04), and albumin (P less than .05), as well as in the number of neutrophils (P less than .01). The total number of symptoms reported correlated significantly with the net increase in the concentration of kinins (r = .549; P less than .01), albumin (r = .674; P less than .001), TAME-esterase activity (r = .563; P less than .005), and neutrophils (r = .605; P less than .005). Levels of histamine did not change during the course of infection. During symptomatic rhinovirus infections (1) kinins are generated, (2) vascular permeability increases, (3) basophils and mast cells do not participate, and (4) neutrophils enter nasal secretions.