DiNovo B B, Doan R, Dyer R B, Baron S, Herzog N K, Niesel D W
Department of Microbiology and Immunology, University of Texas Medical Branch, Galveston 77555-1019, USA.
FEMS Immunol Med Microbiol. 1996 Sep;15(2-3):149-58. doi: 10.1111/j.1574-695X.1996.tb00066.x.
Pathogenesis mediated by Shigella flexneri requires invasion of the gastrointestinal epithelium. It has been previously shown that HeLa cells challenged with S. flexneri show alterations in their phosphotyrosine-containing protein profile. In this report, we demonstrated that bacterial water extracts (WE) abrogated the invasion of HeLa cells by S. flexneri in a dose-dependent manner. A proteinaceous component of S. flexneri was shown to be responsible for this inhibitory activity. Proteins encoded on the 140-MDa plasmid were not responsible for the observed inhibition. WE from other Gram-negative bacteria also inhibited Shigella invasion of HeLa cells pretreated with WE showed changes in the profile and the intensity of phosphotyrosine-containing protein bands. These data were consistent with a surface protein component in WE which initiated aberrant host cell signaling at the membrane which may account for the inhibition of bacterial entry.