BACKGROUND: Viral respiratory tract infections may cause both harmless common colds and severe asthma exacerbations; the differences in disease expression probably depend on the allergic status of the patient. To determine whether altered immunologic mechanisms underlie these differences, we investigated nasal inflammation during naturally acquired common cold. METHODS: In a group of 16 patients (eight allergic), nasal brush samples were taken, and nasal symptoms were recorded during common cold, 2 weeks later (convalescence), and at baseline (>4 weeks without nasal symptoms). Nasal brush cells were stained immunohistochemically for Langerhans cells, T cells, monocytes, neutrophils, B cells, macrophages, natural killer (NK) cells, mast cells, eosinophils, eotaxin, and RANTES. RESULTS: Four rhinovirus, four coronavirus, three RSV, one Mycoplasma pneumoniae, and one influenza A/enterovirus double infection were confirmed. Increased numbers of T cells, monocytes, macrophages, NK cells, eosinophils, and RANTES- and eotaxin-positive cells, but not neutrophils, were observed during common cold in allergic and nonallergic patients, and increased numbers of mast cells in allergic patients. Compared to nonallergic patients, in allergic patients eosinophil influx persisted into convalescence. CONCLUSION: Prolonged nasal eosinophil influx was observed in allergic patients after common cold. What immunologic factors can induce prolonged eosinophil influx and whether this may increase the risk of subsequent allergen-induced hypersensitivity reactions must be studied further.