M. Nonaka et al., GM-CSF, IL-8, IL-1R, TNF-ALPHA-R, AND HLA-DR IN NASAL EPITHELIAL-CELLS IN ALLERGIC RHINITIS, American journal of respiratory and critical care medicine, 153(5), 1996, pp. 1675-1681
Citations number
33
Categorie Soggetti
Emergency Medicine & Critical Care","Respiratory System
Epithelial cells potentially contribute to airways inflammation by ant
igen presentation and the production of proinflammatory cytokines. Thi
s study investigated the immunocytochemical localization of interleuki
n-8 (IL-8), granulocyte-macrophage colony-stimulating factor (GM-CSF),
interleukin-1 receptor (IL-1R Type I), tumor necrosis factor-alpha re
ceptor (TNF-alpha R; 55kD), and human leukocyte antigen-DR (HLA-DR) on
epithelial cells obtained by nasal brushing from 10 patients with all
ergic rhinitis in season and 15 healthy, nonallergic subjects. Six of
the 15 nonallergic asymtomatic subjects had macroscopic evidence of na
sal mucosal inflammation, and their brushings contained more than 10%
neutrophils (''sub-clinical inflammation''). In normal control subject
s, 8 +/- 7.5% of epithelial cells stained for HLA-DR, approximately on
e quarter stained for IL-8 and GM-CSF, and about one third stained pos
itive for IL-1R and TNF-alpha R. The findings in subjects with allergi
c rhinitis in season and with subclinical neutrophilia were similar, a
nd the numbers of cells staining for HLA-DR, IL-8, GM-CSF, IL-1R, and
TNF-alpha R were significantly greater than in normal control subjects
. In nonallergic subjects, GM-CSF and IL-8 expression correlated signi
ficantly with neutrophil content; HLA-DR expression correlated with bo
th neutrophil and lymphocyte content. These findings further support t
he conclusion that epithelial cells can contribute to inflammatory pro
cesses in the nasal mucosa. The findings emphasize the need to identif
y asymptomatic nasal mucosal inflammation in studies of the nasal muco
sa.