Lower airways inflammation in allergic rhinitics: a comparison with asthmatics and normal controls

Background: allergic rhinitis (AR) and asthma represent a continuum of atopic disease. AR is believed to pre-dispose an individual to asthma. Compared with asthmatics and normal controls, the inflammatory response in the lower airways of rhinitics is not fully elucidated. To test the hypothesis that the inflammatory response in the airways of subjects with AR is at a level intermediate between that in normal controls and asthmatics, we have characterized bronchial inflammation and cytokine mRNA levels in non-asthmatic allergic rhinitics and compared it with subjects with allergic asthma and with normal controls.Methods: endobronchial mucosal biopsies were obtained at bronchoscopy from 14 allergic rhinitics, 16 asthmatics and 21 normal controls. Biopsies were embedded into glycol methacrylate resin for immunohistochemical analysis of cellular inflammation and snap frozen for semi-quantitative PCR analysis of cytokine mRNA levels.Results: airway inflammation in rhinitic subjects was characterized by an increase in submucosal eosinophils, mast cells and the mRNA expression of TNF-?, at an intermediate level between healthy and asthmatics. In addition, CD3+ and CD8+ lymphocytes in the epithelium, the endothelial expression of vascular adhesion molecule-1 and IL-1? mRNA were higher in the allergic rhinitics compared with both normal controls and asthmatics, whereas growth-related oncogene ?-mRNA was decreased in AR compared with both healthy and asthmatics. Airway inflammation in the asthmatic group was characterized by higher numbers of eosinophils and mast cells, together with an increase in TNF-?-mRNA compared with both healthy and rhinitics. IFN-? mRNA was the highest in normal controls and lowest in the asthmatics.Conclusions: tn individuals with AR the present data suggest an intermediate state of airway inflammation between that observed in normal individuals and subjects with clinical asthma. It is also indicated that IFN-? production by CD8+ T lymphocytes could be protective against the development of airway hyperresponsiveness. Further work is needed to evaluate this hypothesi