Recent advances in Helicobacter pylori pathogenesis

Sibony, Michal; Jones, Nicola L.

doi:10.1097/mog.0b013e32834dda51

Cited by 43 publications

(42 citation statements)

References 26 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…H. pylori produces several important virulence molecules that interact with epithelial cells and immune cells. The cag pathogenicity island (PAI) encodes type 4 secretion systems that inject CagA into target cells upon attachment (9)(10)(11). After CagA injection, CagA undergoes tyrosine phosphorylation and causes actin-cytoskeletal rearrangements, proliferation of host cells, and interleukin 8 (IL-8) release, all factors important for disease development.…”

mentioning

confidence: 99%

Lactobacilli Reduce Helicobacter pylori Attachment to Host Gastric Epithelial Cells by Inhibiting Adhesion Gene Expression

et al. 2016

View full text Add to dashboard Cite

The human gastrointestinal tract, including the harsh environment of the stomach, harbors a large variety of bacteria, of which Lactobacillus species are prominent members. The molecular mechanisms by which species of lactobacilli interfere with pathogen colonization are not fully characterized. In this study, we aimed to study the effect of lactobacillus strains upon the initial attachment of Helicobacter pylori to host cells. Here we report a novel mechanism by which lactobacilli inhibit adherence of the gastric pathogen H. pylori. In a screen with Lactobacillus isolates, we found that only a few could reduce adherence of H. pylori to gastric epithelial cells. Decreased attachment was not due to competition for space or to lactobacillus-mediated killing of the pathogen. Instead, we show that lactobacilli act on H. pylori directly by an effector molecule that is released into the medium. This effector molecule acts on H. pylori by inhibiting expression of the adhesin-encoding gene sabA. Finally, we verified that inhibitory lactobacilli reduced H. pylori colonization in an in vivo model. In conclusion, certain Lactobacillus strains affect pathogen adherence by inhibiting sabA expression and thereby reducing H. pylori binding capacity.

show abstract

mentioning

confidence: 99%

Lactobacilli Reduce Helicobacter pylori Attachment to Host Gastric Epithelial Cells by Inhibiting Adhesion Gene Expression

et al. 2016

View full text Add to dashboard Cite

show abstract

“…Its spiral shape and unipolar flagella give the pathogen the motility critically needed to colonize and persist in the gastric lumen. H. pylori has developed unique sets of genetic and physiological tools to survive and grow in the extremes of the human gastric environment (4)(5)(6)(7)(8). Moreover, it can transform itself from a helical bacillary morphology to a viable but nonculturable coccoid form under oxidative stress and in ageing cultures (9).…”

mentioning

confidence: 99%

Intracellular Locations of Replication Proteins and the Origin of Replication during Chromosome Duplication in the Slowly Growing Human Pathogen Helicobacter pylori

Sharma

Kamran

Verma

et al. 2013

Journal of Bacteriology

View full text Add to dashboard Cite

bWe followed the position of the replication complex in the pathogenic bacterium Helicobacter pylori using antibodies raised against the single-stranded DNA binding protein (HpSSB) and the replicative helicase (HpDnaB). The position of the replication origin, oriC, was also localized in growing cells by fluorescence in situ hybridization (FISH) with fluorescence-labeled DNA sequences adjacent to the origin. The replisome assembled at oriC near one of the cell poles, and the two forks moved together toward the cell center as replication progressed in the growing cell. Termination and resolution of the forks occurred near midcell, on one side of the septal membrane. The duplicated copies of oriC did not separate until late in elongation, when the daughter chromosomes segregated into bilobed nucleoids, suggesting sister chromatid cohesion at or near the oriC region. Components of the replication machinery, viz., HpDnaB and HpDnaG (DNA primase), were found associated with the cell membrane. A model for the assembly and location of the H. pylori replication machinery during chromosomal duplication is presented.

show abstract

“…9 The pathogenic mechanisms underlying the positive relationship detected between H. pylori infection and CRD have not yet been clarified. 25 One theory suggests that the persistent inflammatory airway response induced by mediators released during H. pylori infection leads to the development of CRD. 10,26 Another possible pathogenic mechanism is the increased sensitivity of lung cells and bronchial tissue to external stimulants such as smoke and dust induced by H. pylori infection in the lung, 9 thus increasing CRD morbidity.…”

Section: Discussionmentioning

confidence: 99%

Association Between Chronic Respiratory Diseases and Helicobacter pylori: A Meta-Analysis

Wang

Guan

et al. 2015

Archivos de Bronconeumología (English Edition)

View full text Add to dashboard Cite

Recent advances in Helicobacter pylori pathogenesis

Cited by 43 publications

References 26 publications

Lactobacilli Reduce Helicobacter pylori Attachment to Host Gastric Epithelial Cells by Inhibiting Adhesion Gene Expression

Lactobacilli Reduce Helicobacter pylori Attachment to Host Gastric Epithelial Cells by Inhibiting Adhesion Gene Expression

Intracellular Locations of Replication Proteins and the Origin of Replication during Chromosome Duplication in the Slowly Growing Human Pathogen Helicobacter pylori

Association Between Chronic Respiratory Diseases and Helicobacter pylori: A Meta-Analysis

Contact Info

Product

Resources

About