CagA tyrosine phosphorylation and interleukin-8 induction by Helicobacter pylori are independent from AlpAB, HopZ and Bab group outer membrane proteins

Odenbreit, Stefan; Kavermann, Holger; Puls, Jürgen; Haas, Rainer

doi:10.1078/1438-4221-00205

Cited by 67 publications

(65 citation statements)

References 50 publications

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“…One possibility is that BabA (but not BabB) is immunogenic in rhesus macaques and that loss of babA reflects antigenic variation that the bacterium uses to avoid the host immune response. To examine this, we purified partial fragments of recombinant BabA and BabB as described (24). By ELISA we were unable to demonstrate seroreactivity to either BabA or BabB up to 5 months after inoculation in the monkeys from which we isolated J166 output , although as expected they did demonstrate increased seroreactivity to H. pylori wholecell antigen (Fig.…”

Section: Discussionmentioning

confidence: 75%

Modification of Helicobacter pylori outer membrane protein expression during experimental infection of rhesus macaques

Solnick

Hansen

Salama

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

217

216

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Clinical isolates of Helicobacter pylori show marked diversity, which may derive from genomic changes that occur during the often lifelong association of the bacterium with its human host. We used the rhesus macaque model, together with DNA microarrays, to examine genomic changes in H. pylori that occur early during experimental infection. Microarray analysis showed that H. pylori recovered from challenged macaques had deleted babA, a member of a large family of paralogous outer membrane proteins (OMPs) that mediates attachment of H. pylori to the Lewis B blood group antigen on gastric epithelium. In some cases the babA gene was replaced by babB, an uncharacterized OMP that is closely related to babA. In other cases the babA gene was present but was not expressed because of alteration in dinucleotide CT repeats in the 5 coding region. In either case, strains lacking babA did not adhere to Lewis B, which is expressed on macaque gastric epithelium. Absence of babA and duplication of babB was also seen in H. pylori isolates derived from human clinical samples, suggesting that this gene conversion event is not unique to experimentally infected rhesus monkeys. These results demonstrate in real time with a relevant animal model that H. pylori regulates OMP expression in vivo by using both antigenic variation and phase variation. We suggest that changes in babA and babB after experimental infection of macaques represent a dynamic response in the H. pylori outer membrane that facilitates adherence to the gastric epithelium and promotes chronic infection.

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Section: Discussionmentioning

confidence: 75%

Modification of Helicobacter pylori outer membrane protein expression during experimental infection of rhesus macaques

Solnick

Hansen

Salama

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

217

216

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“…Blots were developed with the ECL reagents (Amersham Biosciences). The tyrosine phosphorylation status of CagA in infected AGS cells was examined as previously described (10).…”

Section: Methodsmentioning

confidence: 99%

“…The function of AlpAB is unclear partly due to conflicting data regarding the effect of alpAB isogenic mutants on IL-8 induction from epithelial cells (10,12). Previous studies used alpAB mutants constructed by either transposon shuttle mutagenesis of alpA or insertion of the kanamycin resistance cassette into the gene (8 -12).…”

mentioning

confidence: 99%

Functional and Intracellular Signaling Differences Associated with the Helicobacter pylori AlpAB Adhesin from Western and East Asian Strains

Lü

Beswick³

et al. 2007

Journal of Biological Chemistry

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“…Immunoblotting was performed using standard methods. Anti-BabA antiserum (AK277) 33 was used as the primary antibody at a 1:5000 dilution. Horseradish-peroxidase-conjugated protein A (1:3000) (Bio-Rad Laboratory, Hercules, CA) was used as the secondary antibody.…”

Section: Detection Of Baba Protein and Lewis B Antigen Bindingmentioning

confidence: 99%

“…The specificity of this antiserum for BabA during immunoblotting was confirmed previously. 33 For semiquantitation, 4, 2, and 0.5 μg of J99 strain protein extracts were transferred to each membrane, and the density of the band detected in the 4-μg sample from each strain was expressed numerically using the Image J 1.36 software from the National Institutes of Health (available at: http://rsbweb.nih.gov/ij/). We generated a standard curve using extracts from the J99 strain, and the density of bands detected in the samples from each strain was expressed as the percentage density relative to the J99 strain 4-μg sample.…”

Section: Detection Of Baba Protein and Lewis B Antigen Bindingmentioning

confidence: 99%

Helicobacter pylori BabA Expression, Gastric Mucosal Injury, and Clinical Outcome

Fujimoto¹,

Ojo²,

Arnqvist³

et al. 2007

Clinical Gastroenterology and Hepatology

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101

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CagA tyrosine phosphorylation and interleukin-8 induction by Helicobacter pylori are independent from AlpAB, HopZ and Bab group outer membrane proteins

Cited by 67 publications

References 50 publications

Modification of Helicobacter pylori outer membrane protein expression during experimental infection of rhesus macaques

Modification of Helicobacter pylori outer membrane protein expression during experimental infection of rhesus macaques

Functional and Intracellular Signaling Differences Associated with the Helicobacter pylori AlpAB Adhesin from Western and East Asian Strains

Helicobacter pylori BabA Expression, Gastric Mucosal Injury, and Clinical Outcome

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