Airway Inflammation in Atopic Patients: Comparison of Upper & Lower Airway

Abstract

Allergic rhinitis (AR) and asthma represent a continuum of atopic disease and frequently occur as co-morbid conditions in the same patients. The precise mechanism underlying the inflammatory response in the lower airways of rhinitics is not fully elucidated. The primary objective of our study was to understand and to assess the inflammatory response within the upper and lower airways in patients suffering with both asthma and allergic rhinitis. METHODS: Endobronchial and nasal biopsies were obtained from atopic patients with mild asthma and persistent allergic rhinitis. Single blinded study was carried out between April 2007-July 2008. Coded biopsy specimens were embedded into glycol methacrylate resin for immunohistochemical analysis using monoclonal antibodies directed against specific cell markers including mast cells (AA1), eosinophils (EG2), neutrophils (NOE), lymphocytes (CD3ϩ, CD4ϩ, CD8ϩ). 10 analyzable biopsy specimens were studied. Cells were counted blind, as cells/mm2 both in the epithelium and the submucosal matrix. MannWhitney U-test was used for analyses. P-values of 0.05 were considered to be statistically significant. RESULTS: There was a significant increase in CD4ϩ, CD8ϩ cell counts (pϽ0.05) in lower airway. There were no differences between the two groups in the numbers of neutrophils, mast cells, eosinophils and the CD3ϩ cell counts. CONCLUSIONS: The upper airway had a similar pattern of mast cells, neutrophils and eosinophils to that in the lower airway. The increased CD4ϩ lymphocytes may be important in development and maintenance of allergic disease in the lower airway while the CD8 suggests functional diversity and protective effects in the lower airway.

Upper and lower airway remodelling mechanisms in asthma, allergic rhinitis and chronic rhinosinusitis: The one airway concept revisited

“…71 Paired upper and lower airway bronchoscopic samples from patients with AR and allergic asthma confirm similar Th2 cell-driven inflammation in the nasal and bronchial mucosa. 72 If the linear model that inflammation leads to remodelling is followed, then persistent structural changes should be key findings in AR as is the case in asthma.…”

Clinical and immunological phenoendotypes of rhinitis

“…После активации TLRs рецепторов эпителиальных клеток происходит выделение эйкозаноидов, эндопептидаз, цитокинов и хемокинов (IL-6, IL-8, IL-25, IL31 и др., GM-CSF, TNF-α, RANTES, ТАКП и др. ), что способствует повышению аллергического воспаления [2]. Кроме того, назальные эпителиальные клетки продуцируют металлопротеиназы ММР-2, ММР-9 и ММР-13, которые могут расщеплять практически все секретируемые медиаторы и молекулы клеточной поверхности, а также внеклеточный матрикс.…”

Disease models of chronic inflammatory airway disease

“…Despite the 'united airways' concept, allergen challenges in different airway compartments model different aspects of the allergic airway inflammation and subsequent changes in physiology, based on local differences in anatomy, histopathology (airway remodeling), key inflammatory mediators and the associated response to therapy [37][38][39]. Therefore, allergen challenges of different airway compartments are not (fully) interchangeable.…”