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Departments of
*
Medicine and
Pediatrics and Molecular Microbiology, Washington University School of Medicine, St. Louis, MO 63110
Epithelial cells interact directly with bacteria in the environment
and play a critical role in airway defense against microbial pathogens.
In this study, we examined the response of respiratory epithelial cells
to infection with nontypable Haemophilus influenzae.
Using an in vitro cell culture model, we found that epithelial cell
monolayers released significant quantities of IL-8 and expressed
increased levels of ICAM-1 mRNA and surface protein in response to
H. influenzae. In contrast, levels of IL-1ß, TNF-
,
and MHC class I were not significantly affected, suggesting
preferential activation of a specific subset of epithelial genes
directed toward defense against bacteria. Induction of ICAM-1 required
direct bacterial interaction with the epithelial cell surface and was
not reproduced by purified H. influenzae
lipooligosaccharide. Consistent with a functional role for this
response, induction of ICAM-1 by H. influenzae mediated
increased neutrophil adherence to the epithelial cell surface.
Furthermore, in an in vivo murine model of airway infection with
H. influenzae, increased epithelial cell ICAM-1
expression coincided with increased chemokine levels and neutrophil
recruitment in the airway. These results indicate that ICAM-1
expression on human respiratory epithelial cells is induced by
epithelial cell interaction with H. influenzae and
suggest that an ICAM-1-dependent mechanism can mediate neutrophil
adherence to these cells independent of inflammatory mediator release
by other cell types. Direct induction of specific epithelial cell genes
(such as ICAM-1 and IL-8) by bacterial infection may allow for rapid
and efficient innate defense in the airway.
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