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1 Department of Geriatric
Medicine and 2 Department of
Otorhinolaryngology,
To further
understand the early biochemical events that occur in infected surface
epithelium, we developed for the first time a model in which a
respiratory submucosal gland cell population can be infected with
rhinovirus (RV). Viral infection was confirmed by demonstrating with
PCR that viral titers in supernatants and lysates from infected cells
increased with time. Infection by RV14 upregulated the expression of
intercellular adhesion molecule-1 (ICAM-1) mRNA, the major RV receptor,
on submucosal gland cells, and it increased production of interleukin
(IL)-1
, IL-1
, IL-6, IL-8, tumor necrosis factor-
, and
granulocyte-macrophage colony-stimulating factor in supernatants.
Antibodies to ICAM-1 inhibited RV infection of submucosal gland cells
and decreased the production of cytokines after RV infection. Both
IL-1
and IL-1
upregulated ICAM-1 mRNA expression and increased
susceptibility to RV infection, whereas other cytokines failed to alter
ICAM-1 mRNA expression. Furthermore, neutralizing antibodies to IL-1
and IL-1
significantly decreased the viral titers in supernatants
and ICAM-1 mRNA expression after RV infection, but a neutralizing
antibody to tumor necrosis factor-
was without effect. These
findings suggest that respiratory submucosal gland cells play an
important role in the initial stages of inflammation and provide useful
insights into the pathogenesis of RV infection.
intercellular adhesion molecule-1; asthma; common cold; airway inflammation; interleukin-1; polymerase chain reaction
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