Glomerular endothelial cell injury mediated by shiga-like toxin-1

Kidney & Blood Pressure Research
S Adler, R Bollu

Abstract

The hemolytic uremic syndrome is an important cause of acute renal failure and is often associated with prior infection with enterotoxigenic strains of Escherichia coli. Significant pathologic changes in the glomerulus include endothelial cell swelling, detachment, and intravascular coagulation. We investigated the potential pathogenetic mechanisms of this disease by exposing cultured rat glomerular endothelial cells to shiga-like toxin 1 (SLT-1). Glomerular endothelial cell viability and protein synthesis were not affected by 10(-9) M SLT-1. Synthesis and release of thromboxane (Tx) A2, measured as the stable metabolite TxB2, and of 12-(S)-HETE were each increased 1.6 +/- 0.1 fold (p < 0.05). No change was observed in the production of PGE2 or 6-keto-PGF1 alpha, the active metabolite of PGI2. SLT-1 (10(-9) M) significantly increased cell retraction and the formation of gaps in the glomerular endothelial cell monolayer for up to 6 h following exposure. A similar effect was seen with 0.1 microM 12-(S)-HETE. SLT-1 and 0.01 microM 12-(S)-HETE also significantly decreased adhesion of glomerular endothelial cells to fibronectin (75 +/- 4 and 65 +/- 2% of control, respectively; p < 0.001) and laminin (81 +/- 5 and 67 +/- 4% of contro...Continue Reading

Citations

May 30, 2001·Microbes and Infection·E V O'Loughlin, R M Robins-Browne
Jun 9, 2000·Kidney International·K E Meyers, B S Kaplan
Aug 23, 2002·The New England Journal of Medicine·Joel L Moake
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Mar 31, 2010·Infection and Immunity·Dinorah Leyva-IlladesVernon L Tesh
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Jul 28, 2020·Prostaglandins, Leukotrienes, and Essential Fatty Acids·Youjia DuPeter Zahradka

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