The Caenorhabditis elegans ABL-1 tyrosine kinase is required for Shigella flexneri pathogenesis.

Journal Article

Shigellosis is a diarrheal disease caused by the gram-negative bacterium Shigella flexneri. Following ingestion of the bacterium, S. flexneri interferes with innate immunity, establishes an infection within the human colon, and initiates an inflammatory response that results in destruction of the tissue lining the gut. Examination of host cell factors required for S. flexneri pathogenesis in vivo has proven difficult due to limited host susceptibility. Here we report the development of a pathogenesis system that involves the use of Caenorhabditis elegans as a model organism to study S. flexneri virulence determinants and host molecules required for pathogenesis. We show that S. flexneri-mediated killing of C. elegans correlates with bacterial accumulation in the intestinal tract of the animal. The S. flexneri virulence plasmid, which encodes a type III secretory system as well as various virulence determinants crucial for pathogenesis in mammalian systems, was found to be required for maximal C. elegans killing. Additionally, we demonstrate that ABL-1, the C. elegans homolog of the mammalian c-Abl nonreceptor tyrosine kinase ABL1, is required for S. flexneri pathogenesis in nematodes. These data demonstrate the feasibility of using C. elegans to study S. flexneri pathogenesis in vivo and provide insight into host factors that contribute to S. flexneri pathogenesis.

Full Text

Duke Authors

Cited Authors

  • Burton, EA; Pendergast, AM; Aballay, A

Published Date

  • July 2006

Published In

Volume / Issue

  • 72 / 7

Start / End Page

  • 5043 - 5051

PubMed ID

  • 16820504

International Standard Serial Number (ISSN)

  • 0099-2240

Digital Object Identifier (DOI)

  • 10.1128/AEM.00558-06

Language

  • eng

Conference Location

  • United States