Advanced search
Start date
Betweenand

Dynamics of pedestal formation by atypical Enteropathogenic Escherichia coli strains displaying distinct actin polymerization pathways

Grant number: 16/08401-2
Support type:Scholarships abroad - Research Internship - Doctorate
Effective date (Start): September 01, 2016
Effective date (End): February 28, 2017
Field of knowledge:Biological Sciences - Microbiology
Principal Investigator:Waldir Pereira Elias Junior
Grantee:Fernando Henrique Martins
Supervisor abroad: Vanessa Sperandio
Home Institution: Instituto Butantan. Secretaria da Saúde (São Paulo - Estado). São Paulo , SP, Brazil
Local de pesquisa : University of Texas Southwestern Medical Center, Dallas (UT Southwestern), United States  
Associated to the scholarship:13/17403-0 - Role of EspFu protein on atypical Enteropathogenic Escherichia coli, BP.DR

Abstract

Atypical enteropathogenic Escherichia coli (aEPEC) is one of the most important pathogen causing diarrhea disease worldwide. The hallmark of aEPEC pathogenesis is the ability to cause attaching and effacing (A/E) lesions on intestinal epithelium, a property triggered by proteins encoded on a pathogenicity island called locus of enterocyte effacement (LEE). The A/E phenotype is a dynamic process that requires a timely and coordinate expression of the bacterial virulence machinery, and aEPEC strains can induce A/E lesions using distinct pathways. However, the dynamics of A/E lesions formation and the host responses to aEPEC strains with distinct abilities for actin polymerization are poorly characterized. Thus, the aim of this study is to compare the dynamics of pedestal formation by aEPEC strains displaying distinct actin polymerization patterns, as well analyze the transcriptional profiles of the host cells to these processes. Therefore, it will be performed the kinetics of pedestal formation induced by these aEPEC strains employing HeLa-adherence and fluorescente actin staining (FAS) assays, as well time-lapse microscopy. Further, it will be quantified the expression of virulence genes involved in the A/E phenotype during the course of infection. Finally, it will be analyzed the transcriptional profiles of HeLa cells infected with these different aEPEC strains. Thus, we intend to better understand the divergent actin pedestal formation patterns displayed by aEPEC strains, as well provide new insights on pathogenesis of this important group of enteropathogens.