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J. Biol. Chem., Vol. 277, Issue 15, 13346-13353, April 12, 2002
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From the During apical colonization by Salmonella
typhimurium, intestinal epithelial cells orchestrate a
proinflammatory response that involves secretion of chemoattractants,
predominantly interleukin-8, which coordinate neutrophil
trans-epithelial migration at the site of infection. This host-pathogen
interaction requires several S. typhimurium genes. To
identify novel genes that participate in this pathogen-induced
proinflammatory response, we created S. typhimurium Tn-10
transposon mutants and identified a single mutant with Tn-10
insertional inactivation within the fliE flagellar locus
that was able to adhere to and invade intestinal epithelial cells
normally but was unable to induce interleukin-8 secretion in host
cells. The fliE-deficient mutant failed to secrete
flagellin and lacked any surface assembly of flagellae. Unlike
wild-type S. typhimurium, the fliE-deficient
mutant did not activate the I
The Salmonella typhimurium Flagellar Basal Body
Protein FliE Is Required for Flagellin Production and to Induce a
Proinflammatory Response in Epithelial Cells*
§,§¶,
,,,,,
Department of Pathology and Laboratory
Medicine, Emory University, Atlanta, Georgia 30322, the
Department of Veterinary Pathobiology, Texas A & M University,
College Station, Texas 77843, and ** Unité de
Pathogénie Microbienne Moléculaire,
Paris Cédex 15, France
B
/NF-B signaling pathway or
induce the coordinated trans-epithelial migration of isolated human
neutrophils. Transcomplementation of the fliE-deficient
mutant with a wild-type fliE-harboring plasmid restored all
defects and produced a wild-type S. typhimurium phenotype. Furthermore, functional down-regulation of basolateral TLR5 completely inhibited the monolayers' ability to respond to both wild-type S. typhimurium and purified flagellin but had no affect on
tumor necrosis factor -induced responses. We therefore conclude that S. typhimurium fliE is essential for flagellin secretion,
flagellar assembly, and S. typhimurium-induced
proinflammatory responses through basolateral TLR5 and is consistent
with the emerging model of S. typhimurium flagellin-induced inflammation.
*
This work was supported by National Institutes of Health
Grants DK-10085 (to M. E. H.) and DK-35932 and DK-47622 (to
J. L. M.).The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.
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