PubTransformer

A site to transform Pubmed publications into these bibliographic reference formats: ADS, BibTeX, EndNote, ISI used by the Web of Knowledge, RIS, MEDLINE, Microsoft's Word 2007 XML.

A hemolytic-uremic syndrome-associated strain O113:H21 Shiga toxin-producing Escherichia coli specifically expresses a transcriptional module containing dicA and is related to gene network dysregulation in Caco-2 cells.

Abstract Shiga toxin-producing (Stx) Escherichia coli (STEC) O113:H21 strains are associated with human diarrhea and some of these strains may cause hemolytic uremic syndrome (HUS). The molecular mechanism underlying this capacity and the differential host cell response to HUS-causing strains are not yet completely understood. In Brazil O113:H21 strains are commonly found in cattle but, so far, were not isolated from HUS patients. Here we conducted comparative gene co-expression network (GCN) analyses of two O113:H21 STEC strains: EH41, reference strain, isolated from HUS patient in Australia, and Ec472/01, isolated from cattle feces in Brazil. These strains were cultured in fresh or in Caco-2 cell conditioned media. GCN analyses were also accomplished for cultured Caco-2 cells exposed to EH41 or Ec472/01. Differential transcriptome profiles for EH41 and Ec472/01 were not significantly changed by exposure to fresh or Caco-2 conditioned media. Conversely, global gene expression comparison of both strains cultured in conditioned medium revealed a gene set exclusively expressed in EH41, which includes the dicA putative virulence factor regulator. Network analysis showed that this set of genes constitutes an EH41 specific transcriptional module. PCR analysis in Ec472/01 and in other 10 Brazilian cattle-isolated STEC strains revealed absence of dicA in all these strains. The GCNs of Caco-2 cells exposed to EH41 or to Ec472/01 presented a major transcriptional module containing many hubs related to inflammatory response that was not found in the GCN of control cells. Moreover, EH41 seems to cause gene network dysregulation in Caco-2 as evidenced by the large number of genes with high positive and negative covariance interactions. EH41 grows slowly than Ec472/01 when cultured in Caco-2 conditioned medium and fitness-related genes are hypoexpressed in that strain. Therefore, EH41 virulence may be derived from its capacity for dysregulating enterocyte genome functioning and its enhanced enteric survival due to slow growth.
PMID
Related Publications

Genetic diversity and virulence potential of shiga toxin-producing Escherichia coli O113:H21 strains isolated from clinical, environmental, and food sources.

Prevalence and characterization of Shiga toxin-producing Escherichia coli isolated from cattle, food, and children during a one-year prospective study in France.

Characterization and Virulence Potential of Serogroup O113 Shiga Toxin-Producing Escherichia coli Strains Isolated from Beef and Cattle in the United States.

Set of virulence genes and genetic relatedness of O113 : H21 Escherichia coli strains isolated from the animal reservoir and human infections in Brazil.

Serotypes, virulence markers and cell invasion ability of Shiga toxin-producing Escherichia coli strains isolated from healthy dairy cattle.

Authors

Mayor MeshTerms
Keywords
Journal Title plos one
Publication Year Start




PMID- 29253906
OWN - NLM
STAT- In-Process
LR  - 20171224
IS  - 1932-6203 (Electronic)
IS  - 1932-6203 (Linking)
VI  - 12
IP  - 12
DP  - 2017
TI  - A hemolytic-uremic syndrome-associated strain O113:H21 Shiga toxin-producing
      Escherichia coli specifically expresses a transcriptional module containing dicA 
      and is related to gene network dysregulation in Caco-2 cells.
PG  - e0189613
LID - 10.1371/journal.pone.0189613 [doi]
AB  - Shiga toxin-producing (Stx) Escherichia coli (STEC) O113:H21 strains are
      associated with human diarrhea and some of these strains may cause hemolytic
      uremic syndrome (HUS). The molecular mechanism underlying this capacity and the
      differential host cell response to HUS-causing strains are not yet completely
      understood. In Brazil O113:H21 strains are commonly found in cattle but, so far, 
      were not isolated from HUS patients. Here we conducted comparative gene
      co-expression network (GCN) analyses of two O113:H21 STEC strains: EH41,
      reference strain, isolated from HUS patient in Australia, and Ec472/01, isolated 
      from cattle feces in Brazil. These strains were cultured in fresh or in Caco-2
      cell conditioned media. GCN analyses were also accomplished for cultured Caco-2
      cells exposed to EH41 or Ec472/01. Differential transcriptome profiles for EH41
      and Ec472/01 were not significantly changed by exposure to fresh or Caco-2
      conditioned media. Conversely, global gene expression comparison of both strains 
      cultured in conditioned medium revealed a gene set exclusively expressed in EH41,
      which includes the dicA putative virulence factor regulator. Network analysis
      showed that this set of genes constitutes an EH41 specific transcriptional
      module. PCR analysis in Ec472/01 and in other 10 Brazilian cattle-isolated STEC
      strains revealed absence of dicA in all these strains. The GCNs of Caco-2 cells
      exposed to EH41 or to Ec472/01 presented a major transcriptional module
      containing many hubs related to inflammatory response that was not found in the
      GCN of control cells. Moreover, EH41 seems to cause gene network dysregulation in
      Caco-2 as evidenced by the large number of genes with high positive and negative 
      covariance interactions. EH41 grows slowly than Ec472/01 when cultured in Caco-2 
      conditioned medium and fitness-related genes are hypoexpressed in that strain.
      Therefore, EH41 virulence may be derived from its capacity for dysregulating
      enterocyte genome functioning and its enhanced enteric survival due to slow
      growth.
FAU - Bando, Silvia Yumi
AU  - Bando SY
AD  - Department of Pediatrics, Faculdade de Medicina da Universidade de Sao Paulo
      (FMUSP), Sao Paulo, SP, Brazil.
FAU - Iamashita, Priscila
AU  - Iamashita P
AD  - Department of Pediatrics, Faculdade de Medicina da Universidade de Sao Paulo
      (FMUSP), Sao Paulo, SP, Brazil.
FAU - Guth, Beatriz E
AU  - Guth BE
AD  - Departament of Microbiology, Immunology and Parasitology, Universidade Federal de
      Sao Paulo, Escola Paulista de Medicina, Sao Paulo, SP, Brazil.
FAU - Dos Santos, Luis F
AU  - Dos Santos LF
AD  - Departament of Microbiology, Immunology and Parasitology, Universidade Federal de
      Sao Paulo, Escola Paulista de Medicina, Sao Paulo, SP, Brazil.
FAU - Fujita, Andre
AU  - Fujita A
AD  - Department of Computer Science, Instituto de Matematica e Estatistica,
      Universidade de Sao Paulo, Sao Paulo, SP, Brazil.
FAU - Abe, Cecilia M
AU  - Abe CM
AD  - Laboratory of Bacteriology, Butantan Institute, Sao Paulo, SP, Brazil.
FAU - Ferreira, Leandro R
AU  - Ferreira LR
AD  - Department of Pediatrics, Faculdade de Medicina da Universidade de Sao Paulo
      (FMUSP), Sao Paulo, SP, Brazil.
FAU - Moreira-Filho, Carlos Alberto
AU  - Moreira-Filho CA
AUID- ORCID: http://orcid.org/0000-0003-3433-4714
AD  - Department of Pediatrics, Faculdade de Medicina da Universidade de Sao Paulo
      (FMUSP), Sao Paulo, SP, Brazil.
LA  - eng
PT  - Journal Article
DEP - 20171218
PL  - United States
TA  - PLoS One
JT  - PloS one
JID - 101285081
PMC - PMC5734773
EDAT- 2017/12/19 06:00
MHDA- 2017/12/19 06:00
CRDT- 2017/12/19 06:00
PHST- 2017/07/20 00:00 [received]
PHST- 2017/11/29 00:00 [accepted]
PHST- 2017/12/19 06:00 [entrez]
PHST- 2017/12/19 06:00 [pubmed]
PHST- 2017/12/19 06:00 [medline]
AID - 10.1371/journal.pone.0189613 [doi]
AID - PONE-D-17-27117 [pii]
PST - epublish
SO  - PLoS One. 2017 Dec 18;12(12):e0189613. doi: 10.1371/journal.pone.0189613.
      eCollection 2017.