Premium
Cellular infiltration and cytokine mRNA expression in perennial allergic rhinitis
Author(s) -
Varga EM,
Jacobson MR,
Till SJ,
Masuyama K,
O'Brien F,
Durham SR,
Rak S,
Lund V,
Scadding GK,
Hamid QA
Publication year - 1999
Publication title -
allergy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.363
H-Index - 173
eISSN - 1398-9995
pISSN - 0105-4538
DOI - 10.1034/j.1398-9995.1999.00957.x
Subject(s) - eosinophil , cytokine , immunology , tryptase , eosinophilia , interleukin 5 , infiltration (hvac) , mast cell , medicine , allergy , pathology , interleukin , asthma , physics , thermodynamics
Background: Allergen challenge in allergic rhinitis patients leads to local eosinophilia and Th2‐type cytokine expression. Natural exposure to grass pollen is additionally characterized by epithelial mast‐cell infiltration. We hypothesized that perennial allergic rhinitis is also associated with T‐cell and eosinophil infiltration of the nasal mucosa, local Th2‐type cytokine expression, and increased numbers of nasal epithelial mast cells. Methods: Nasal biopsies from perennial allergic rhinitis patients and controls were analysed by immunocytochemistry for different cell populations and in situ hybridization for cytokine mRNA‐expressing cells. Results: Perennial allergic rhinitis was associated with increased numbers of submucosal CD3+ T cells ( P =0.05), EG2+ activated eosinophils ( P =0.01), and CD68+ macrophages ( P =0.01) compared to controls. Epithelial, but not submucosal, tryptase‐positive mast cells were also elevated in rhinitics compared to controls ( P =0.01). The numbers of cells expressing interleukin (IL)‐5 were higher ( P =0.01) and the numbers of cells expressing IL‐2 were lower ( P =0.04) in rhinitic patients than controls. There were no significant differences for either IL‐4 or interferon‐gamma between the groups. Conclusions: Perennial allergic rhinitis is characterized by mast‐cell migration into the epithelium; submucosal infiltration by T cells, eosinophils, and macrophages; and an imbalance in local T‐cell cytokine production in favour of enhanced IL‐5 and reduced IL‐2 expression.