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Rhinovirus (RV) infections appear to precipitate most asthma exacerbations. To investigate whether RV-16 induces different inflammatory changes in upper and lower airways of asthmatic and healthy subjects, we inoculated 10 nonatopic healthy and 11 atopic asthmatic adults with 2,000 TCID50 RV-16. Subjects recorded symptoms and peak flow daily; and they underwent spirometry, methacholine challenge (PC20), nasal lavage, and sputum induction at baseline and on Days 2, 4, 15, and 29 d after inoculation. One asthmatic subject developed an exacerbation requiring prednisone treatment 5 d after inoculation. The cold symptom severity (Jackson score) did not differ between groups. During the cold, asthma symptoms increased slightly from baseline in the asthmatic group; and PC20 decreased in the healthy group. However, peak flow, bronchodilator use, and spirometry did not change in either group. At baseline, asthmatics had higher neutrophils, eosinophils, and interleukin (IL)-6 in nasal lavage. After inoculation, both groups developed significant increases in nasal neutrophils, IL-6 and IL-8, and modest increases in sputum neutrophils and IL-6, but not IL-8. However, these changes did not differ between groups. IL-5, interferon-gamma, and RANTES were detected only in nasal lavages from two asthmatic subjects, who had the most severe colds. IL-11 was not detected in any sample. We conclude that inflammatory responses of upper and lower airways during RV-16 colds are similar in asthmatic and healthy subjects, and that RV-16 infection is not by itself sufficient to provoke clinical worsening of asthma.

A humanized murine monoclonal antibody directed to the Fc epsilonR1-binding domain of human IgE (rhuMAb-E25) has been shown to inhibit the binding of IgE to mast cells without provoking mast cell activation. To examine the effects of neutralizing IgE on allergic airway responses, we assessed the effects of 9 wk of treatment with rhuMAb-E25 in a parallel group, randomized, double-blind, placebo-controlled study of 19 allergic asthmatic subjects. We found that treatment with rhuMAb-E25 reduced serum IgE, increased the dose of allergen needed to provoke an early asthmatic response, reduced the mean maximal fall in FEV1 during the early response (30 +/- 10% at baseline to 18.8 +/- 8%, versus 33 +/- 8% at baseline to 34 +/- 4% after placebo; p = 0.01), and reduced the mean maximal fall in FEV1 during the late response (24 +/- 20% at baseline to 9 +/- 10% versus 20 +/- 17% at baseline to 18 +/- 17% after placebo; p = 0.047). We conclude that an anti-IgE monoclonal antibody, which inhibits binding of IgE to its receptor, suppresses the early- and late-phase responses to inhaled allergen in allergic asthmatic subjects. Targeting IgE with rhuMAb-E25 might be a useful treatment for allergic asthma.