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B Through a Lipopolysaccharide-Dependent Innate Intracellular Response and Leads to IL-8 Expression in Epithelial Cells1
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Unité de Pathogénie Microbienne Moléculaire, Institut National de la Santé et de la Recherche Médicale, Unité 389, and
Unité de Biologie Moléculaire de l’Expression Génique, Unité de Recherche Associée 1773 Centre National de la Recherche Scientifique, Institut Pasteur, Paris, France
The pathogenesis of Shigella flexneri infection
centers on the ability of this organism to invade epithelial cells and
initiate an intense inflammatory reaction. Because NF-
B is an
important transcriptional regulator of genes involved in inflammation,
we investigated the role of this transcription factor during S.
flexneri infection of epithelial cells. Infection of HeLa cells
with invasive S. flexneri induced NF-B DNA-binding
activity; noninvasive S. flexneri strains did not lead
to this activation. The pathway leading to NF-B activation by
invasive S. flexneri involved the kinases,
NF-B-inducing kinase, IB kinase-1, and IB kinase-2. NF-B
activation was linked to inflammation, because invasive S.
flexneri activated an IL-8 promoter-driven reporter gene, and
the B site within this promoter was indispensable for its induction.
Microinjection of bacterial culture supernatants into HeLa cells
suggested that LPS is responsible for NF-B activation by S.
flexneri infection. In conclusion, the eukaryotic transcription
factor NF-B was activated during S. flexneri
infection of epithelial cells, which suggests a role for this
transcriptional regulator in modulating the immune response during
infection in vivo.
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