We investigated the pathophysiology of rhinovirus colds by challenging volunteers with either of two strains of rhinovirus or with placebo. Nasal lavagesweredone before challenge and every 4 h for five days after challenge. We measured the levels of histamine, kinins, [³H]-N-α-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 infectedand symptomatic showed increases in levels of kinins (P <.03), TAME-esterase activity (P <.04), and albumin (P <.05), as well as in the number of neutrophils (P < .01). The total number of symptoms reported correlated significantly with the net increase in the concentration of kinins (r = .549; P <.01), albumin (r = .674; P < .001), TAME-esterase activity (r = .563; P <.005),and neutrophils (r = .605; P <.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.