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Shiga Toxin Type 1 Activates Tumor Necrosis Factor- Gene
Transcription and Nuclear Translocation of the Transcriptional
Activators Nuclear Factor- B and Activator Protein-1
Ramesh Sakiri,
Belakere Ramegowda, and
Vernon L. Tesh
From the Department of Medical Microbiology and Immunology, Texas A&M
University Health Science Center, College Station, TX.
Shiga toxins (Stxs) produced by Shigella dysenteriae 1 and
Escherichia coli have been implicated in the pathogenesis of
bloody diarrhea, acute renal failure, and neurologic abnormalities. The pathologic hallmark of Stx-mediated tissue damage is the development of
vascular lesions in which endothelial cells are swollen and detached
from underlying basement membranes. However, in vitro studies using
human vascular endothelial cells demonstrated minimal Stx-induced
cytopathic effects, unless the target cells were also incubated with
the proinflammatory cytokines tumor necrosis factor- (TNF-) or
interleukin-1 (IL-1). These cytokines have been shown to
upregulate the expression of the Stx-binding membrane glycolipid globotriaosylceramide (Gb3). We show here that purified
Stx1 induces TNF secretion by a human monocytic cell line, THP-1, in a
dose- and time-dependent manner. Treatment of cells with both
lipopolysaccharides (LPS) and Stx1 results in augmented TNF production.
Treatment with the nontoxic Gb3-binding subunit of Stx1 or
with an anti-Gb3 monoclonal antibody did not trigger TNF
production. Northern blot analyses show that Stx1 causes increased
TNF- production through transcriptional activation. Increased levels
of TNF- mRNA are preceded by the nuclear translocation of the
transcriptional activators NF- B and AP-1 and the loss of cytoplasmic
IB-. These data are the first to show that, in addition to direct
cytotoxicity, Stxs possess cellular signaling capabilities sufficient
to induce the synthesis of cytokines that may be necessary for target
cell sensitization and the development of vascular lesions.
Blood, Vol. 92 No. 2 (July 15), 1998:
pp. 558-566
© 1998 by the American Society of Hematology.
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