Abstract
Enteropathogenic Escherichia coli (EPEC) is a known causative agent of diarrhea in children. In the process of colonization of the small intestine, EPEC synthesizes two types of adhesins, the bundle-forming pilus (BFP) and intimin. The BFP pilus is an adhesin associated with the initial stages of adherence of EPEC to epithelial cells, while the outer membrane protein intimin carries out the intimate adherence that takes place at the third stage of infection. BFP is encoded by the bfp operon located in plasmid EAF, present only in typical EPEC isolates, while eae, the gene that encodes intimin is situated in the LEE, a chromosomal pathogenicity island. Transcription of bfp and eae is regulated by the products of the perABC operon, also present in plasmid EAF. Here we show that deletion of relA, that encodes a guanosine penta and tetraphosphate synthetase impairs EPEC adherence to epithelial cells in vitro. In the absence of relA, the transcription of the regulatory operon perABC is reduced, resulting in lower levels of BFP and intimin. Bacterial adherence, BFP and intimin synthesis and perABC expression are restored upon complementation with the wild-type relA allele.
Highlights
Enteropathogenic Escherichia coli (EPEC) is one of the causes of infant diarrhea in developing countries [1,2]
The bfp operon is formed by 14 genes that are associated with the biogenesis of the bundle-forming pilus (BFP), a type IV fimbria found in typical EPEC strains [4]. bfpA, the first gene of the operon encodes the main subunit of the fimbria
We show that deletion of relA impairs bacterial adherence, reduces the synthesis of the adhesins BFP and intimin and inhibits the transcription of the perABC operon
Summary
Enteropathogenic Escherichia coli (EPEC) is one of the causes of infant diarrhea in developing countries [1,2]. Typical EPEC cells form microcolonies on epithelial cell monolayers, a pattern known as localized adherence (LA) [3]. These strains carry a large plasmid known as EAF, which harbors two operons, bfp and perABC (or per), needed to confer on EPEC the LA phenotype. The second stage of EPEC infection is characterized by the secretion of bacterial effector via a type III secretion system into the host cell followed by the corruption of the host signal transduction. Many genes associated with EPEC virulence are present in the LEE, including the ones encoding the type III secretion system, the secreted proteins and the adhesin intimin. In typical EPEC, transcription of the bfp operon and of the LEE genes are activated, respectively, by PerA and PerC, encoded by the perABC operon [11,12]
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