Airway inflammation in asthma and perennial allergic rhinitis. Relationship with nonspecific bronchial responsiveness and maximal airway narrowing

Background: Eosinophilic airway inflammation is the hallmark of asthma, but it has also been reported in other conditions such as allergic rhinitis. W e have tested whether the analysis of cells and chemicals in sputum can dis tinguish between patients with mild allergic asthma, those with allergic rh initis, and healthy controls. The relationship between inflammation markers in sputum and nonspecific bronchial hyperresponsiveness to methacholine (B HR) (PD20 and maximal response plateau [MRP] values) was also evaluated. Methods: We selected 31 mild asthmatics and 15 rhinitis patients sensitized to house-dust mite. As a control group, we studied 10 healthy subjects. Ev ery subject underwent the methacholine bronchial provocation test (M-BPT) a nd sputum induction. Blood eosinophils and serum ECP levels were measured. Sputum cell differentials were assessed, and eosinophil cationic protein (E CP), tryptase, albumin, and interleukin (IL)-5 levels were measured in the entire sputum supernatant. Results: Blood eosinophils and serum ECP levels were higher in asthma patie nts and rhinitis than in healthy controls, but no difference: between asthm a patients and rhinitis patients was found. Asthmatics had higher eosinophi l counts and higher ECP and tryptase levels in sputum than rhinitis patient s or control subjects. Sputum albumin levels were higher in asthmatics than in controls. Rhinitis patients exhibited higher sputum eosinophils than he althy controls. An association between sputum eosinophil numbers and MPR va lues (r = -0.57) was detected, and a trend toward correlation between sputu m ECP levels and PD20 values (r = -0.47) was found in the rhinitis group, b ut not in asthmatics. No correlation between blood eosinophilic inflammatio n and lung functional indices was found. Conclusions: Induced sputum is an accurate method to study bronchial inflam mation, allowing one to distinguish between rhinitis patients and mildly as thmatic patients. The fact that no relationship was detected between sputum inflammation and BHR suggests that other factors, such as airway remodelin g, may be at least partly responsible for BHR in asthma.