HorB (HP0127) is a gastric epithelial cell adhesin

Typeset version

 

TY  - JOUR
  - Snelling, WJ,Moran, AP,Ryan, KA,Scully, P,McGourty, K,Cooney, JC,Annuk, H,O'Toole, PW
  - 2007
  - June
  - Helicobacter
  - HorB (HP0127) is a gastric epithelial cell adhesin
  - Validated
  - ()
  - Helicobacter pylori adhesion HorB lipopolysaccharide HELICOBACTER-PYLORI INFECTION OUTER-MEMBRANE PROTEINS BLOOD-GROUP ANTIGENS ESCHERICHIA-COLI POLYACRYLAMIDE GELS LEWIS-X DUODENAL-ULCER SYDNEY STRAIN MOUSE MODEL AGS CELLS
  - 12
  - 200
  - 209
  - Background: The Helicobacter pylori protein HorB (encoded by HP0127) is a member of a paralogous family that includes the adhesins BabA, AlpA, AlpB, and HopZ, which contribute to adhesion to gastric epithelial cells. Of the verified H. pylori porins, the HorB sequence is most similar to that of HopE, but the function of HorB is unknown. The aim of our study was to investigate the role of HorB in H. pylori gastric epithelial cell adhesion. Materials and methods: We disrupted the horB gene in H. pylori and measured the adhesion to gastric epithelial cells (AGS cells). We then assessed the effect that HorB disruption had on lipopolysaccharide (LPS) O-chain production and Lewis x and Lewis y antigen expression. A HorB mutant in the mouse-adapted strain H. pylori SS1 was created by marker exchange and mouse stomach colonization was quantified. Using reverse transcription polymerase chain reaction, human gastric biopsy material from H. pylori-infected patients was then examined for expression of the horB gene. Results: Disruption of the horB gene reduced H. pylori adhesion by more than twofold. Adhesion in the horB knockout strain was restored to wild-type levels by re-introduction of HorB into the chromosome. Disruption of HorB reduced production of LPS O-chains and lowered the level of expression of Lewis x and Lewis y antigens. Insertional mutagenesis of the horB gene in H. pylori SS1 reduced mouse stomach colonization threefold. Finally, expression of the horB gene was detected in human gastric biopsy material from H. pylori-infected patients. Conclusions: From these data we conclude that HorB has a role in H. pylori adhesion during infection.
DA  - 2007/06
ER  - 
@article{V43336197,
   = {Snelling,  WJ and Moran,  AP and Ryan,  KA and Scully,  P and McGourty,  K and Cooney,  JC and Annuk,  H and O'Toole,  PW },
   = {2007},
   = {June},
   = {Helicobacter},
   = {HorB (HP0127) is a gastric epithelial cell adhesin},
   = {Validated},
   = {()},
   = {Helicobacter pylori adhesion HorB lipopolysaccharide HELICOBACTER-PYLORI INFECTION OUTER-MEMBRANE PROTEINS BLOOD-GROUP ANTIGENS ESCHERICHIA-COLI POLYACRYLAMIDE GELS LEWIS-X DUODENAL-ULCER SYDNEY STRAIN MOUSE MODEL AGS CELLS},
   = {12},
  pages = {200--209},
   = {{Background: The Helicobacter pylori protein HorB (encoded by HP0127) is a member of a paralogous family that includes the adhesins BabA, AlpA, AlpB, and HopZ, which contribute to adhesion to gastric epithelial cells. Of the verified H. pylori porins, the HorB sequence is most similar to that of HopE, but the function of HorB is unknown. The aim of our study was to investigate the role of HorB in H. pylori gastric epithelial cell adhesion. Materials and methods: We disrupted the horB gene in H. pylori and measured the adhesion to gastric epithelial cells (AGS cells). We then assessed the effect that HorB disruption had on lipopolysaccharide (LPS) O-chain production and Lewis x and Lewis y antigen expression. A HorB mutant in the mouse-adapted strain H. pylori SS1 was created by marker exchange and mouse stomach colonization was quantified. Using reverse transcription polymerase chain reaction, human gastric biopsy material from H. pylori-infected patients was then examined for expression of the horB gene. Results: Disruption of the horB gene reduced H. pylori adhesion by more than twofold. Adhesion in the horB knockout strain was restored to wild-type levels by re-introduction of HorB into the chromosome. Disruption of HorB reduced production of LPS O-chains and lowered the level of expression of Lewis x and Lewis y antigens. Insertional mutagenesis of the horB gene in H. pylori SS1 reduced mouse stomach colonization threefold. Finally, expression of the horB gene was detected in human gastric biopsy material from H. pylori-infected patients. Conclusions: From these data we conclude that HorB has a role in H. pylori adhesion during infection.}},
  source = {IRIS}
}
AUTHORSSnelling, WJ,Moran, AP,Ryan, KA,Scully, P,McGourty, K,Cooney, JC,Annuk, H,O'Toole, PW
YEAR2007
MONTHJune
JOURNAL_CODEHelicobacter
TITLEHorB (HP0127) is a gastric epithelial cell adhesin
STATUSValidated
TIMES_CITED()
SEARCH_KEYWORDHelicobacter pylori adhesion HorB lipopolysaccharide HELICOBACTER-PYLORI INFECTION OUTER-MEMBRANE PROTEINS BLOOD-GROUP ANTIGENS ESCHERICHIA-COLI POLYACRYLAMIDE GELS LEWIS-X DUODENAL-ULCER SYDNEY STRAIN MOUSE MODEL AGS CELLS
VOLUME12
ISSUE
START_PAGE200
END_PAGE209
ABSTRACTBackground: The Helicobacter pylori protein HorB (encoded by HP0127) is a member of a paralogous family that includes the adhesins BabA, AlpA, AlpB, and HopZ, which contribute to adhesion to gastric epithelial cells. Of the verified H. pylori porins, the HorB sequence is most similar to that of HopE, but the function of HorB is unknown. The aim of our study was to investigate the role of HorB in H. pylori gastric epithelial cell adhesion. Materials and methods: We disrupted the horB gene in H. pylori and measured the adhesion to gastric epithelial cells (AGS cells). We then assessed the effect that HorB disruption had on lipopolysaccharide (LPS) O-chain production and Lewis x and Lewis y antigen expression. A HorB mutant in the mouse-adapted strain H. pylori SS1 was created by marker exchange and mouse stomach colonization was quantified. Using reverse transcription polymerase chain reaction, human gastric biopsy material from H. pylori-infected patients was then examined for expression of the horB gene. Results: Disruption of the horB gene reduced H. pylori adhesion by more than twofold. Adhesion in the horB knockout strain was restored to wild-type levels by re-introduction of HorB into the chromosome. Disruption of HorB reduced production of LPS O-chains and lowered the level of expression of Lewis x and Lewis y antigens. Insertional mutagenesis of the horB gene in H. pylori SS1 reduced mouse stomach colonization threefold. Finally, expression of the horB gene was detected in human gastric biopsy material from H. pylori-infected patients. Conclusions: From these data we conclude that HorB has a role in H. pylori adhesion during infection.
PUBLISHER_LOCATION
ISBN_ISSN
EDITION
URL
DOI_LINK
FUNDING_BODY
GRANT_DETAILS