Late establishment of the attaching and effacing lesion caused by atypical enteropathogenic Escherichia coli depends on protein expression regulated by Per.
Enteropathogenic Escherichia coli (EPEC) is classified as typical (tEPEC) or atypical (aEPEC) based on the presence or absence of the E. coli adherence factor plasmid (pEAF), respectively. The hallmark of EPEC infection is the formation of the attaching and effacing (A/E) lesions on the gut mucosa. We compared the kinetics of A/E lesion formation induced by aEPEC and tEPEC. The examination of infected HEp-2 cells clearly demonstrated delayed A/E lesion formation by aEPEC in comparison to tEPEC. This delay was associated with the expression of locus of enterocyte effacement (LEE)-encoded virulence factors (i.e., intimin and EspD). Indeed, the insertion of a plasmid containing perABC, a transcriptional regulator of virulence factors involved in A/E formation, into aEPEC strains increased and accelerated the formation of A/E lesions. Interestingly, the enhanced expression and translocation of LEE-encoded proteins, such as those expressed in LEE5 (intimin) and LEE4 (EspD), in aEPEC (perABC) was independent of bacterial adhesion. The secretion kinetics of these two proteins representing LEE5 and LEE4 expression correlated with A/E lesion formation. We conclude that the lack of Per in the regulation network of virulence genes is one of the main factors that delay the establishment of A/E lesions induced by aEPEC strains.
Laboratory of Bacteriology, Instituto Butantan, São Paulo, Brazil.
Vanessa
V
Bueris
Department of Cell Biology, Centro de Investigación y de Estudios Avanzados del IPN, CINVESTAV-IPN, Mexico City, Mexico.
Jazmín
J
Huerta-Cantillo
Department of Cell Biology, Centro de Investigación y de Estudios Avanzados del IPN, CINVESTAV-IPN, Mexico City, Mexico.
Fernando
F
Navarro-Garcia
Laboratory of Bacteriology, Instituto Butantan, São Paulo, Brazil.
Renato M
RM
Ruiz
Laboratory of Genetics, Instituto Butantan, São Paulo, Brazil.
Aurora M
AM
Cianciarullo
Laboratory of Bacteriology, Instituto Butantan, São Paulo, Brazil waldir.elias@butantan.gov.br.
Waldir P
WP
Elias
D018829:Adhesins, Bacterial / Q000235:genetics / Q000378:metabolism*; D001422:Bacterial Adhesion; D054308:Enteropathogenic Escherichia coli / Q000235:genetics / Q000254:growth & development*; D029968:Escherichia coli Proteins / Q000235:genetics / Q000378:metabolism*; D015964:Gene Expression Regulation, Bacterial; D056945:Hep G2 Cells; D022781:Hepatocytes / Q000382:microbiology; D006801:Humans; D010957:Plasmids; D012097:Repressor Proteins / Q000235:genetics / Q000378:metabolism*; D014157:Transcription Factors / Q000235:genetics / Q000378:metabolism*
D018829:Adhesins, Bacterial; D029968:Escherichia coli Proteins; C000595461:PerB protein, E coli; C569462:PerC protein, E coli; D012097:Repressor Proteins; D014157:Transcription Factors; C120886:bfpT protein, E coli; C073819:eaeA protein, E coli