Helicobacter Pylori Vacuolating Research Articles

Causal associations between Helicobacter Pylori infection and the risk and symptoms of Parkinson's disease: a Mendelian randomization study.

Increasing evidence suggests an association between Helicobacter pylori (HP) infection and Parkinson's disease (PD) and its clinical manifestations, but the causal relationship remain largely unknown. To investigate the causal relationship between HP infection and PD risk, PD symptoms, and secondary parkinsonism, we conducted two-sample Mendelian randomization (MR). We obtained summary data from genome-wide association studies for seven different antibodies specific to HP proteins and five PD-related phenotypes. The inverse-variance weighted (IVW), weighted median, weighted mode, and MR-Egger methods were used to assess the causal relationships. Sensitivity analyses were performed to examine the stability of the MR results and reverse MR analysis was conducted to evaluate the presence of reverse causality. Genetically predicted HP antibodies were not causally associated with an increased risk of PD. However, HP cytotoxin-associated gene-A (CagA) and outer membrane protein (OMP) antibody level were causally associated with PD motor subtype (tremor to postural instability/gait difficulty score ratio; β = -0.16 and 0.46, P = 0.002 and 0.048, respectively). HP vacuolating cytotoxin-A (VacA) antibody level was causally associated with an increased risk of PD dementia [odds ratio (OR) = 1.93, P = 0.040]. Additionally, HP OMP antibody level was identified as a risk factor for drug-induced secondary parkinsonism (OR = 2.08, P = 0.033). These results were stable, showed no evidence of heterogeneity or directional pleiotropy, and no evidence of a reverse causal relationship. Our findings indicate that HP infection does not increase the risk of PD, but contributes to PD motor and cognitive symptoms. Different types of HP antibodies affect different symptoms of PD. Eradication of HP infection may help modulate and improve symptoms in PD patients.

Su1929 Delineating the Mechanism for Disruption of Autophagy Maturation by the Helicobacter pylori Vacuolating Cytotoxin a

Su1929 Delineating the Mechanism for Disruption of Autophagy Maturation by the Helicobacter pylori Vacuolating Cytotoxin a

Bioinformatics Analysis on Functional Site and Fingerprint of CagI Protein in <i>Helicobacter pylori</i> Cag Pathogenicity Island

[Objective] This paper aims to make a bioinformatics analysis on the functional site and fingerprint of CagI protein in helicobacter pylori cag pathogenicity island and further explore the functions of CagM protein. [Methods] Use PROSITE SCAN: http://www.expasy.ch/cgi-bin/ prosite/PSScan.cgi server to search the fingerprint sequence of CagI protein and analyze and discuss the possible functions. [Results] The search of PROSITE SCAN found that CagI protein has four kinds of functional sites: N-glycosylation site, protein kinase C phosphorylation site, casein kinase II phosphorylation site, and myristoylation acting site; the search of fingerPRINTScan and printsBLAST server found sixteen fingerprint tags of CagI protein: helicobacter pylori vacuolating toxin tag; flagellin tag; ATP synthetase δ subunit tag; helicobacter pylori outer membrane protein family tag, etc. It is predicted preliminarily that CagI protein also has these functions. [Conclusion] As a kind of secretory protein, CagI protein will be secreted to the outer membrane to form the membrane protein, which will become one part of elicobacter pylori IV type production secretion pilus involved in signal transduction and material transportation and acting as a messenger or carrier, and it many have hydrolase activity and ATP/GTP enzyme activity.*Fund program: National Nature Science Foundation Project (30870096); National Science Foundation Project in Jiangsu Colleges (08KJB310001)

Variants in Autophagy Genes Affect Susceptibility to Both Crohn's Disease and Helicobacter pylori Infection

Helicobacter pylori (H pylori) is a Gram-negative, microaerophilic bacterium that selectively colonizes the stomachs of half the world’s human population. H pylori is the etiologic agent of several gastric diseases, including chronic gastritis and peptic ulcers. Long-term, chronic inflammation subsequently increases the risk for the development of mucosa-associated lymphoid tissue lymphoma and gastric cancer.1,2 During a well-choreographed interaction between the bacteria and the host gastric epithelium, H pylori infection initiates an immune response that leads to a massive infiltration of inflammatory cells.1 An evolutionarily conserved cellular mechanism, autophagy, functions as an innate defense lysosomal pathway in response to infection to degrade intracellular micro-organisms attempting to establish a replicative niche in the host epithelial cell cytoplasm.3 Unfortunately, H pylori utilizes a novel escape mechanism to evade lysosomal destruction in host epithelial cells that subsequently supports chronic infection. A study in this month’s issue of Gastroenterology identifies, for the first time, an autophagy gene as a candidate for host susceptibility to H pylori infection and disease progression.4

T1785 Inhibition of Maturation and Induction of Apoptosis in Dendritic Cell Stimulated With Helicobacter pylori Vacuolating Cytotoxin

T1785 Inhibition of Maturation and Induction of Apoptosis in Dendritic Cell Stimulated With Helicobacter pylori Vacuolating Cytotoxin

T1626 Mechanisms of Apoptosis Induced By vacA, a Helicobacter pylori Vacuolating Cytotoxin

T1626 Mechanisms of Apoptosis Induced By vacA, a Helicobacter pylori Vacuolating Cytotoxin

Helicobacter pylori vaculating cytotoxin inhibits duodenal bicarbonate secretion by a histamine-dependent mechanism

Background & Aims: Helicobacter pylori (HP) infection reduces the secretory capacity of the duodenal mucosa for bicarbonate (Hogan et al. 1996), and CagAVacA positive H.p. extract strongly decreases murine duodenal HCO3- secretion in vitro within one hour (Tuo et al 2004). In this study, we investigated the effect of HP vacuolating cytotoxin (VacA) on duodenal mucosal bicarbonate secretion, and the underlying mechanisms for the VacA-induced reduction in HCO3- secretion.

The Helicobacter pylori vacuolating cytotoxin (VacA) disrupts the epithelial cell cytoskeleton in a strain and cell type specific manner

The Helicobacter pylori vacuolating cytotoxin (VacA) disrupts the epithelial cell cytoskeleton in a strain and cell type specific manner

The Helicobacter pylori vacuolating cytotoxin, VacA, induces both epithelial cell cytoskeletal disruption and vacuolation, but these phenomena are not interdependent

The Helicobacter pylori vacuolating cytotoxin, VacA, induces both epithelial cell cytoskeletal disruption and vacuolation, but these phenomena are not interdependent

Determinants of Helicobacter pylori vacuolating cytotoxin production analysed by construction of vacA hybrids and by site-directed mutagenesis

Determinants of Helicobacter pylori vacuolating cytotoxin production analysed by construction of vacA hybrids and by site-directed mutagenesis