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Department of Medical Microbiology and Immunology, Texas A & M University Health Science Center, College Station, Texas
Correspondence: Vernon L. Tesh, Department of Medical Microbiology and Immunology, Texas A & M University Health Science Center, Rm. 407 Reynolds Medical Building, College Station, TX 77843-1114. E-mail: tesh{at}medicine.tamu.edu
Shiga toxin-producing enterohemorrhagic E. coli infections
cause bloody diarrhea, which may progress to life-threatening
complications such as the hemolytic-uremic syndrome (HUS). HUS patients
frequently have elevated levels of the proinflammatory cytokine tumor
necrosis factor 
(TNF-) detectable in urine. Thus, sequelae may
develop following the localized production of proinflammatory cytokines
within the kidneys. A possible source of these cytokines are
macrophages, which respond to the toxins by producing TNF-. We
have shown previously that THP-1 cells produce soluble TNF- in
response to the toxins, whose production requires host-cell
tyrosine-kinase activity and toxin-enzymatic activity. To further
examine signaling pathways involved in TNF- expression, we
determined that JNK1 and -2 and p38, but not ERK1 or -2, were
phosphorylated following toxin exposure. Blockade of p38 activation
reduced TNF- production following Shiga toxin 1 treatment. Finally,
we present a model of the ribotoxic stress response triggered in human
macrophages by Shiga toxins.
Key Words: cytokines • ERK • HUS • ribosome • signal transduction
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