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Amplifies IL-6 and IL-8 Responses by Airway Epithelial-Like Cells Via Indoleamine 2,3-Dioxygenase1
Departments of
* Pulmonology and
Experimental Immunology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands
Respiratory viral infections increase inflammatory responses to
concurrent or secondary bacterial challenges, thereby worsening disease
outcome. This potentiation of inflammation is explained at least in
part by IFN-
promoting increased sensitivity to TNF-
and LPS. We
sought to determine whether and, if so, how IFN- can modulate
proinflammatory responses to TNF- and LPS by epithelial cells, which
are key effector cells in the airways. Preincubation of airway
epithelial-like NCI-H292 cells with IFN- resulted in a
hyperresponsive IL-6 and IL-8 production to TNF- and LPS. The
underlying mechanism involved the induction of indoleamine
2,3-dioxygenase, which catabolized the essential amino acid,
tryptophan. Depletion of tryptophan led to stabilization of IL-6 and
IL-8 mRNA and increased IL-6 and IL-8 responses, whereas supplementing
tryptophan largely restored these changes. This novel mechanism may be
implicated in enhanced inflammatory responses to bacterial challenges
following viral infection.
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