Role of ENA-78 in helicobacter pylori-associated gastritis

Rieder, Gabriele; Einsiedl, Wolfgang; Hatz, R.; Walz, Antje-Christine; Stolte, M.; Enders, G.

doi:10.1016/s0016-5085(98)84347-3

Cited by 56 publications

(75 citation statements)

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“…In one previous study, IL-8 secretion from epithelial cells could not be detected when adhesion was prevented by separating bacteria from the cells through filter membranes (47). Furthermore, attachment of type 1 H. pylori to epithelial cells leads to a couple of events, such as translocation of CagA into the host cell, induction of signal tranduction pathways, cytoskeletal rearrangements, and cellular growth changes (48).…”

Section: Discussionmentioning

confidence: 96%

TheHelicobacter pyloriBlood Group Antigen-Binding Adhesin Facilitates Bacterial Colonization and Augments a Nonspecific Immune Response

Rad¹,

Gerhard²,

Lang

et al. 2002

The Journal of Immunology

162

104

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Presence of the Helicobacter pylori adherence factor blood group Ag-binding adhesin (BabA; binding to Lewisb (Leb)) is associated with ulcer disease, adenocarcinoma, and precancerous lesions. The importance of BabA for bacterial colonization and the inflammatory response is unknown. A total of 141 antral biopsies from H. pylori-infected patients were assessed in regard to the degree of granulocytic (G0°–G3°) and lymphocytic (L1°–L3°) infiltration. DNA genotypes of babA2 (the transcriptionally active gene of BabA), cagA, and vacAs1/2 were determined by PCR. Colonization density and Leb status on gastric epithelial cells were determined by immunohistochemistry. Real-time quantitative (TaqMan) RT-PCR determined mRNA expression of IL-8, TNF -α, and the Th1 markers IFN-γ and the IL-12R β2 chain. A total of 91% of infected patients were Leb positive. The vacAs1+/cagA+ strains harboring babA2 showed significantly higher levels of granulocytic infiltration, bacterial colonization, and IL-8 mRNA than vacAs1+/cagA+ strains lacking babA2. IL-8 mRNA and protein production by KATO III cells in vitro increased dose dependently with addition of different numbers of type 1 strains (G27 and 2808 strains, 0.1–20 bacteria/cell). The mRNA expression of TNF-α, IFN-γ, and IL-12R β2 was higher in H. pylori-positive patients than in controls, but it did not differ significantly between patients infected with different strain types. These data suggest that BabA facilitates colonization of H. pylori and thereby increases IL-8 response, resulting in enhanced mucosal inflammation. Infection with strains harboring BabA thereby augment a nonspecific immune response, whereas the Th1 response toward H. pylori appears to be independent of BabA, cytotoxin-associated gene A, or vacuolating cytotoxin.

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Section: Discussionmentioning

confidence: 96%

TheHelicobacter pyloriBlood Group Antigen-Binding Adhesin Facilitates Bacterial Colonization and Augments a Nonspecific Immune Response

Rad¹,

Gerhard²,

Lang

et al. 2002

The Journal of Immunology

162

104

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“…A cagE mutant induced only mild inflammation in Mongolian gerbils, whereas the wild-type strain and vacA mutants induced more severe gastritis [30]. Mutation of cagE abolishes the ability of H. pylori to induce the cytokine interleukin-8 (IL-8), a neutrophil chemotactic factor, in Kato-3 cells [27,29,31,32]. Adherence has been shown to play a role in the induction of H. pyloriassociated IL-8 secretion [33].…”

Section: Discussionmentioning

confidence: 99%

Helicobacter pylori adherence to gastric epithelial cells: a role for non-adhesin virulence genes

Zhang¹,

Dorrell

Wren

et al. 2002

Journal of Medical Microbiology

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Helicobacter pylori is a major aetiological agent in gastroduodenal disorders and adherence of the bacteria to the gastric mucosa is one of the initial stages of infection. Although a number of specific adhesins has been identified, other H. pylori virulence factors may play a role in adherence to gastric epithelial cells directly or through interaction with other adhesins. This study assessed the effect of 16 H. pylori virulence factors on the adherence of the bacteria to gastric AGS cells and on gastric epithelial cell cycle distribution. Defined isogenic H. pylori SS1 mutants were used. After coincubation of gastric AGS cells and bacteria, adherence of H. pylori to AGS cells was visualised by immunofluorescence microscopy and quantified by flow cytometry. Cell cycle phase distribution was analysed by flow cytometry with propidium iodide staining. Mutants were tested for their ability to adhere to AGS cells and compared with the wild-type SS1 strain. Mutations in genes in the cag pathogenicity island showed that cagP and cagE mutants adhered less than the wild-type strain to AGS cells, whereas a cagF mutant showed no reduction in adherence. Mutations in genes involved in flagellar biosynthesis showed that the adherence ability of fliQ, f liM and fliS mutants was reduced, but a flhB mutant possessed wild-type levels of adherence. Mutations in genes coding for the urease (ureB) and phospholipase (pldA) enzymes did not affect adherence, but mutation of the tlyA gene encoding an H. pylori haemolysin resulted in a reduced adherence. A fliQ mutant, with reduced adherence to AGS cells, was less able to induce AGS cell apoptosis than SS1. The ability to induce G 0 G 1 cell cycle arrest was also abolished in the fliQ mutant. However, an increased cell number in S phase was observed when AGS cells were exposed to the fliQ mutant compared with SS1, suggesting that unattached bacteria may still be able to stimulate cell proliferation. In addition to known adhesins, other bacterial virulence factors such as CagE, CagP, FliQ, FliM, FliS and TlyA appear to play a role in H. pylori adherence to gastric epithelial cells. Mutations in these genes may affect H. pylori pathogenicity by reducing either the ability of the bacteria to attach to gastric epithelial cells or the intensity of bacteriahost cell interactions.

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“…The cag pathogenicity island (cag PAI) of H. pylori is an important virulence factor that involves several genes with different function in the H. pylori (Crabtree et al, 1995a;Crabtree et al, 1995b;Sharma et al, 1995;Tummuru et al, 1995;Censini et al, 1996;Figura and Valassina, 1999;Asahi et al, 2000;Stein et al, 2000;Megraud, 2001). Adherent of bacterium to gastric epithelial cells is critical to initiate the gastric inflammatory response with different clinical outcomes in humans (Hessey et al, 1990;Logan, 1996;Segal et al, 1996;Rieder et al, 1997). CagL (a VirB5 ortholog) is a bacterial factor that is known as a pilus protein Backert and Selbach, 2008;Backert et al, 2011), Integrin α5β1 is a receptor on gastric epithelial cell that CagL binds to; by its arginineglycine-aspartate (RGD) motif, this interaction activates α5β1 receptor and facilitates the delivery of CagA oncoprotein through type 4 secretion system (T4SS) into the epithelial cell (Parsonnet et al, 1997;Kwok et al, 2007;Backert and Selbach, 2008;Backert et al, 2011;Shaffer et al, 2011).…”

Section: Genotypes Predict Risk Of Peptic Ulcerations But Not Gastricmentioning

confidence: 99%

Helicobacter pylori cag Pathogenicity Island cagL and orf17 Genotypes Predict Risk of Peptic Ulcerations but not Gastric Cancer in Iran

Raei¹,

Latifi‐Navid²,

Zahri³

2015

Asian Pacific Journal of Cancer Prevention

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Background: Gastric cancer (GC) is the third most common cancer regarding mortality in the world. The cag pathogenicity island (PAI) of Helicobacter pylori which contains genes associated with a more aggressive phenotype may involve in the pathogenesis of gastrointestinal disease. We here aimed to examine the associations of cagH, cagL, orf17, and cagG genotypes of H. pylori cag PAI with severe gastrointestinal disease. Materials and Methods: A total of 242 H. pylori strains were genotyped. Histopathological examination and classification of subjects were performed. Results: The frequencies of the cagH, cagL, cagG, and orf17 genotypes were 40/54 (74.1%), 53/54 (98.1%), 38/54 (70.4%), and 43/54 (79.6%), respectively, in patients with peptidic ulceration (PU),while in the control group, the frequencies were 87/147 (59.6%) for cagH, 121/146 (82.9%) for cagL, 109/146 (74.7%) for cagG, and 89/146 (61.0%) for orf17. The results of simple logistic regression analysis showed that the cagL and orf17 genotypes were significantly associated with an increased risk of PU not GC; the ORs (95% CI) were 10.950 (1.446-82.935), and 2.504 (1.193-5.253), respectively. No significant association was found between the cagH and cagG genotypes and the risk of both the PU and the GC in Iran (P>0.05). Finally, multiple logistic regression analysis showed that the cagL genotype was independently and significantly associated with the ageand sex-adjusted risk for PU; the OR (95% CI) was 9.557 (1.219-17.185). Conclusions: We conclude that the orf17 and especially cagL genotypes of H. pylori cag PAI could be factors for risk prediction of PU, but not GC in Iran.

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Role of ENA-78 in helicobacter pylori-associated gastritis

Cited by 56 publications

References 0 publications

TheHelicobacter pyloriBlood Group Antigen-Binding Adhesin Facilitates Bacterial Colonization and Augments a Nonspecific Immune Response

TheHelicobacter pyloriBlood Group Antigen-Binding Adhesin Facilitates Bacterial Colonization and Augments a Nonspecific Immune Response

Helicobacter pylori adherence to gastric epithelial cells: a role for non-adhesin virulence genes

Helicobacter pylori cag Pathogenicity Island cagL and orf17 Genotypes Predict Risk of Peptic Ulcerations but not Gastric Cancer in Iran

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