SummaryBackgroundCold virus infections are associated with asthma attacks and with increased bronchial responsiveness even in normal subjects. Possible mechanisms include epithelial damage, interaction with adhesion molecules or with T‐helper cell subsets.ObjectiveTo determine whether colds increase lower airway inflammation, comparing atopic with non‐atopic normal subjects.MethodsThirty healthy volunteers (15 atopic) took part. Basehne tests included viral serology. microbiological culture and polymerase chain reaction for rhinovirus infection (HRV‐PCR), histamine bronchial provocation and bronchoscopy. Twenty subjects (eight atopic) underwent repeat tests when they developed a cold.ResultsForced expiratory volume in one second (FEV1) was significantly lower during colds (‐0.19L 95 confidence mterval ‐0.10, ‐0.29,P= 0,0004) and there was a significant increase in bronchial responsiveness (+0.62 doublings of the dose‐response slope +0.24, +1.00,P=0.003). Eight subjects (two atopic) had a diagnosed viral infection: two HRV. three coronavirus (HCV), one HRV + HCV, one parainfluenza III(PI) and one respiratory syncytial virus (RSV) (alsoHaemophilus influenzae). In biopsies, during colds, total eosinophils (EG1+) increased significantly (geometric mean 6.73‐fold 1.12,40.46,P=O.04). Activated eosinophils (EG2+) only increased significantly in the subgroup without diagnosed viral infection and particularly in atopic rhinitics. T‐suppressor (CD8+) cells also increased significantly (median +178.3 cells mm2,P= 0.004). Epithelial expression of intercellular adhesion molecule‐1 (ICAM‐1) expression increased in four atopic rhinitics during colds. Bronchial washings showed a significant increase in neutrophils (GM 1.53‐fold 1.04,2.25,P= 0.02).ConclusionLower airway inflammation was present in atopic and non‐atopic normal subjects with colds. Atopic subjects differed in that they were less likely to have positive virological tests and were more likely to show activated eosinophilia in the lower airway, despite a sim
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