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Infection and Immunity, February 1999, p. 800-804, Vol. 67, No. 2
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.
Bacterial Invasion Is Not Required for
Activation of NF-
B in Enterocytes
Tonyia
Eaves-Pyles,
Csaba
Szabó, and
Andrew L.
Salzman*
Division of Critical Care, Children's
Hospital Medical Center, Cincinnati, Ohio 45229
Received 1 June 1998/Returned for modification 29 July
1998/Accepted 19 November 1998
Pathogenic enteric microorganisms induce the NF-
B-dependent
expression of proinflammatory genes in intestinal epithelial cells. The
purpose of the present study was to clarify the contribution of
microbial invasion to the degradation of the regulatory protein I
B
and the subsequent activation of NF-
B in cultured
intestinal epithelial cells. Caco-2BBe cells were incubated with
Salmonella dublin, Salmonella typhimurium,
or a weakly invasive strain of E. coli.
S. dublin and S. typhimurium (107
organisms/ml) induced equivalent concentration-dependent gel mobility
shifts of an NF-
B consensus sequence that was preceded by I
B
degradation. E. coli (107 organisms/ml) did not
induce I
B
degradation or NF-
B translocation. Pretreatment with
cytochalasin D blocked invasion of all three strains but had no effect
on I
B
degradation or NF-
B activation. S. dublin
and S. typhimurium adhered to Caco-2BBe cells 3- to 10-fold
more than E. coli. NF-
B activation was prevented by
physical separation of S. dublin from Caco-2BBe cells by a
0.4-µm-pore-size filter. Our results imply that bacterial adhesion,
rather than invasion or release of a secreted factor, is sufficient to
induce I
B
degradation and NF-
B activation in intestinal
epithelial cells. Our data suggest that strategies to reduce enteric
inflammation should be directed to the reduction of bacterial
enterocyte adhesion.
*
Corresponding author. Mailing address: Inotek
Corporation, Third Floor, 3130 Highland Ave., Cincinnati, OH
45219-2374. Phone: (513) 475-6655. Fax: (513) 221-8079. E-mail:
alsalzman{at}aol.com.
Infection and Immunity, February 1999, p. 800-804, Vol. 67, No. 2
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.
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