The Caenorhabditis elegans ABL-1 Tyrosine Kinase Is Required for Shigella flexneri Pathogenesis. Export

@article{citeulike:3325775, abstract = {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.}, author = {Burton, E. A. and Pendergast, A. M. and Aballay, A.}, citeulike-article-id = {3325775}, citeulike-linkout-0 = {http://view.ncbi.nlm.nih.gov/pubmed/16820504}, citeulike-linkout-1 = {http://www.hubmed.org/display.cgi?uids=16820504}, citeulike-linkout-2 = {http://www.wormbase.org/db/misc/paper?name=WBPaper00027729}, journal = {Appl Environ Microbiol}, keywords = {abl-1, article, c\_elegans, caenorhabditis\_elegans, celegans, elegans, m791, nematode, wormbase}, pages = {5043--5051}, posted-at = {2008-09-23 22:57:20}, priority = {3}, title = {The Caenorhabditis elegans ABL-1 Tyrosine Kinase Is Required for Shigella flexneri Pathogenesis.}, url = {http://view.ncbi.nlm.nih.gov/pubmed/16820504}, volume = {72}, year = {2006} }

TY - JOUR ID - citeulike:3325775 L3 - citeulike-article-id:3325775 N2 - 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. JF - Appl Environ Microbiol EP - 5051 TI - The Caenorhabditis elegans ABL-1 Tyrosine Kinase Is Required for Shigella flexneri Pathogenesis. VL - 72 SP - 5043 KW - abl-1 KW - article KW - c_elegans KW - caenorhabditis_elegans KW - celegans KW - elegans KW - m791 KW - nematode KW - wormbase AU - Burton, EA AU - Pendergast, AM AU - Aballay, A PY - 2006/// UR - http://view.ncbi.nlm.nih.gov/pubmed/16820504 ER -