Latrunculin B facilitates Shiga toxin 1 transcellular transcytosis across T84 intestinal epithelial cells

Irina Maluykova, Oksana Gutsal, Marina Laiko, Anne Kane, Mark Donowitz, Olga Kovbasnjuk

Research output: Contribution to journalArticlepeer-review


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.

Original languageEnglish (US)
Pages (from-to)370-377
Number of pages8
JournalBiochimica et Biophysica Acta - Molecular Basis of Disease
Issue number6
StatePublished - Jun 2008


  • Actin turnover
  • Intestinal epithelial cells
  • Latrunculin B
  • Shiga toxin
  • Transcytosis

ASJC Scopus subject areas

  • Molecular Medicine
  • Molecular Biology


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