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Investigation of the variability of type 1 pili in biofilm formation and aggregative adherence pattern in atypical enteropathogenic Escherichia coli isolates

Grant number: 25/06479-3
Support Opportunities:Scholarships in Brazil - Scientific Initiation
Start date: June 01, 2025
End date: November 30, 2025
Field of knowledge:Biological Sciences - Microbiology - Biology and Physiology of Microorganisms
Principal Investigator:Rodrigo Tavanelli Hernandes
Grantee:Francisco José de Moraes Bassetto
Host Institution: Instituto de Biociências (IBB). Universidade Estadual Paulista (UNESP). Campus de Botucatu. Botucatu , SP, Brazil
Associated research grant:17/14821-7 - Exploring novel virulence strategies in Escherichia coli, AP.TEM

Abstract

Enteropathogenic Escherichia coli (EPEC) is one of the six pathotypes of diarrheagenic E. coli (DEC). EPEC is defined by the presence of a pathogenicity island called the locus of enterocyte effacement (LEE region). The LEE region harbors a set of genes responsible for encoding proteins involved in the biogenesis of a type 3 secretion system, effector proteins, and the afimbrial adhesin intimin. Some EPEC isolates also carry a high-molecular-weight adherence plasmid (pEAF), with those harboring this plasmid classified as typical (tEPEC), while isolates lacking this plasmid are known as atypical (aEPEC). Among the many virulence factors present in E. coli isolates, type 1 pili (T1P) stands out as a fimbriae belonging to the chaperone-usher family. The major protein (pilin) of this fimbria is called FimA, while the protein that binds to mannosylated glycoproteins present in eukaryotic cells is known as FimH. Previous studies have shown that antigenic variability in the FimH protein can interfere with its efficiency in recognizing mannosylated eukaryotic receptors, as well as in biofilm formation. A previous study from our laboratory demonstrated that an aEPEC isolate of serotype O2:H16, harboring the fimH24 variant, was capable of producing the aggregative adherence (AA) pattern-characterized by the organization of bacterial cells adhering to epithelial cells and/or the glass surface of coverslips in a manner resembling a stacked brick wall-only in adherence assays performed in the absence of D-mannose. This finding suggests a possible contribution of T1P to the establishment of this phenotype. Thus, the objective of the present study is to evaluate whether the antigenic variability of the FimH protein has a direct relationship with the establishment of the AA pattern, as well as with biofilm formation by aEPEC isolates obtained from children and adults with diarrhea in Brazil. (AU)

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