Key points are not available for this paper at this time.
Human rhinoviruses (HRV) are an important cause of upper respiratory tract infection and are etiologically linked with asthma exacerbations. However, the mechanisms of virus-induced inflammation are largely unknown. We examined nasal mucosal biopsies for the presence of an associated inflammatory cellular infiltrate during experimental rhinovirus infection. A group of 21 adult volunteers (10 atopic) had baseline nasal biopsies, followed 2 wk later by inoculation with HRV Serotype 16. Nasal biopsies were taken on Day 4 of the cold and again 6-10 wk later. Infection was documented by symptom scores, viral culture, and seroconversion. The biopsies were fixed in acetone and processed into glycol methacrylate resin for semithin sectioning. Mast cells, eosinophils, lymphocytes, and neutrophils were identified with appropriate monoclonal antibodies and a streptavidin-biotin horseradish peroxidase technique. There were no significant changes in the numbers of inflammatory cells present during the cold or the convalescent period compared with baseline biopsies (Wilcoxon paired, p > 0.05). There were also no differences between normal and atopic groups. We suggest that rhinoviral colds are not associated with increased inflammatory cellularity and that other mechanisms, such as increased mediator release, are responsible for coryzal symptoms.
Fraenkel et al. (Sat,) studied this question.