| Grant number: | 16/17584-3 |
| Support Opportunities: | Scholarships abroad - Research |
| Start date: | August 15, 2017 |
| End date: | February 14, 2018 |
| Field of knowledge: | Biological Sciences - Microbiology - Biology and Physiology of Microorganisms |
| Principal Investigator: | Rodrigo Tavanelli Hernandes |
| Grantee: | Rodrigo Tavanelli Hernandes |
| Host Investigator: | David A. Rasko |
| Host Institution: | Instituto de Biociências (IBB). Universidade Estadual Paulista (UNESP). Campus de Botucatu. Botucatu , SP, Brazil |
| Institution abroad: | University of Maryland, Baltimore (UMB), United States |
Abstract Atypical enteropathogenic E.coli (aEPEC) are one of the most prevalent diarrheagenic E. coli pathotype implicated as a cause of diarrhea in children and adults worldwide. The hallmark of aEPEC infection is the formation of a lesion termed attaching and effacing (AE) lesion, which promotes the intimate adherence of the bacteria to the host cells, erasure of brush border microvilli and formation of a pedestal-like structure rich in F-actin. The proteins necessary to modify the host cells leading to the AE lesion formation are encoded by genes located on a pathogenicity island termed LEE region. The LEE region encodes a Type III secretion system (T3SS). Unlike typical EPEC, aEPEC lack the EPEC adherence factor plasmid (pEAF), which harbors the genes associated with the bundle forming pilus (BFP) biogenesis, and consequently, aEPEC do not exhibit localized adherence (LA) on the infected epithelial cells surface. Besides the effector proteins encoded by genes from the LEE region, additional effectors, that interact with several cellular processes and could increase the severity of diarrheal disease, are delivered to the host cells via T3SS. The objective of the present study is to perform whole-genome sequence of 100 aEPEC strains, isolated in Brazil in recent years, in order to understand their phylogenetic origin, the diversity of LEE types, and to draw a picture of the virulence strategies employed by aEPEC to colonize and damage the host. Additionally we will examine the prevalence of plasmids that could contribute to the virulence of these strains. These data will be utilized to improve the diagnosis strategies employed for aEPEC identification in the routine laboratory, and lead discovery of new putative virulence markers and plasmids for further characterization. (AU) | |
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