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1 Pulmonary and Critical Care
Medicine Section,
Interleukin (IL)-4 is thought to contribute to the
Th2 type of immune response and hence the development of allergic
reactions such as asthma. In asthmatic patients, the airway epithelium
expresses increased amounts of the cell surface adhesion molecule
intercellular adhesion molecule (ICAM)-1 (CD54). One cytokine capable
of inducing ICAM-1 in airway epithelial cells, tumor necrosis
factor-
(TNF-), is present in asthma. This study evaluated if
IL-4 either alone or together with TNF- costimulation might modulate
CD54 expression by human bronchial epithelial cells (HBECs). CD54
positivity increased in response to IL-4 (16 ± 2% positive vs. 3 ± 1%, P < 0.01); greater induction of CD54 resulted from TNF- (45 ± 2%,
P < 0.001). Costimulation with
TNF- plus IL-4 further augmented expression (56 ± 1%,
P < 0.05). Immunoperoxidase results
were confirmed by flow cytometry. RT-PCR revealed no increase in ICAM-1
mRNA expression under control conditions or after stimulation with IL-4
alone. TNF- increased IL-4 mRNA, and IL-4 potentiated this.
Functionally, IL-4 augmented the adhesion of THP-1 monocyte/macrophage
cells to monolayers of HBECs both alone and in the presence of TNF-.
We conclude that 1) IL-4 augments
epithelial cell ICAM-1 expression,
2) IL-4 potentiates the adhesion of
THP-1 monocyte/macrophage cells to epithelial cells, and
3) modulation of epithelial cell
ICAM-1 expression by IL-4 may play a role in the immunopathology of
bronchial asthma.
interleukin-4; interleukin-10; interleukin-13; intercellular
adhesion molecule-1; tumor necrosis factor-
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