Journal
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE
Volume 1782, Issue 6, Pages 370-377Publisher
ELSEVIER
DOI: 10.1016/j.bbadis.2008.01.010
Keywords
Shiga toxin; intestinal epithelial cells; transcytosis; actin turnover; latrunculin B
Funding
- NCRR NIH HHS [S10 RR022551-01A1] Funding Source: Medline
- NIDDK NIH HHS [R01 DK058928, R01 DK058928-03, R24 DK064388, R01DK58928, P30 DK034928, R24DK064388, P30DK 34928] Funding Source: Medline
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Shiga toxins (Stx), released into the intestinal lumen by enterohemorrhagic Escherichia coli (EHEC), are major virulence factors responsible for gastrointestinal and systemic illnesses. These pathologies are believed to be due to the action of the toxins on endothelial cells, which express the Stx receptor, the glycosphingolipid Gb3. To reach the endothelial cells, Stx must translocate across the intestinal epithelial monolayer. This process is poorly understood. We investigated Stx1 movement across the intestinal epithelial T84 cell model and the role of actin turnover in this transcytosis. We showed that changes in the actin cytoskeleton due to latrunculin B, but not cytochalasin D or jasplakinolide, significantly facilitate toxin transcytosis across T84 monolayers. This trafficking is transcellular and completely inhibited by tannic acid, a cell impermeable plasma membrane fixative. This indicates that actin turnover could play an important role in Stx1 transcellular transcytosis across intestinal epithelium in vitro. Since EHEC attachment to epithelial cells causes an actin rearrangement, this finding may be highly relevant to Stx-induced disease. (C) 2008 Elsevier B.V. All rights reserved
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