Gastric mucosal hydrophobicity in duodenal ulceration: Role of Helicobacter pylori infection density and mucus lipids

Asante, Maxwell A.; Ahmed, Hafez; Patel, Praful; Davis, Tracy L.; Finlayson, C.; Mendall, Michael A.; Northfield, T. C.

doi:10.1053/gast.1997.v113.pm9247463

Cited by 33 publications

(15 citation statements)

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“…22 It has recently been reported23 that GMSH in antral biopsy specimens of infected patients was inversely related to the bacterial density in antral histology; in our sample this association was confirmed only in middle aged subjects. In addition we have established for the first time that in humans GMSH decreases with age independently of H pylori status, the effect being seen equally in infected and uninfected individuals.…”

Section: Discussionsupporting

confidence: 58%

Age and Helicobacter pylori decrease gastric mucosal surface hydrophobicity independently

Hackelsberger

Platzer

Nilius

et al. 1998

Gut

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Background-Gastric mucosal surface hydrophobicity (GMSH) is an essential component of the mucosal defence system that is decreased by Helicobacter pylori and non-steroidal anti-inflammatory drugs (NSAIDs). Gastric ulcers occur predominantly in elderly subjects, and may thus reflect diminished mucosal resistance. Aims-To investigate whether aging decreases GMSH. Patients-One hundred and twenty patients without peptic ulcer disease were divided into three age groups: I (41 years or below); II (41-64 years); and III (65 years or above). Methods-Biopsy specimens were taken from the antrum, corpus, and cardia for histology (Sydney system), urease testing for H pylori, and for contact angle measurement of GMSH with a goniometer. The presence of specific H pylori antibodies was checked by immunoblotting. Results-Fifty two patients (43%) were infected, and 68 were uninfected with H pylori. GMSH at all biopsy sites was lower in H pylori infected subjects (p=0.0001), but also decreased with age independently of infection status (p=0.0001). The most notable decrease in GMSH occurred between age groups I and II in those with, and between age groups II and III in those without, H pylori infection. GMSH was greater in antral than in corpus mucosa in both infected (p=0.0001) and uninfected patients (p=0.0003). Conclusions-A physiological decrease in GMSH with aging may contribute to the risk of ulcer development in the elderly, and may act synergistically with H pylori and/or NSAIDs on gastric mucosal defence. (Gut 1998;43:465-469)

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Section: Discussionsupporting

confidence: 58%

Age and Helicobacter pylori decrease gastric mucosal surface hydrophobicity independently

Hackelsberger

Platzer

Nilius

et al. 1998

Gut

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“…Phospholipids constitute c. 20% of the dry weight of the human gastric mucus and are believed to be important in generating a hydrophobic barrier and maintaining normal cell functions. It has been reported that mucosal hydrophobicity is reduced in H. pylori-positive patients with duodenal ulcer compared with those having gastritis only [48]. The significantly diminished induction of apoptosis and cell cycle arrest by the pldA mutant suggests that H. pylori phospholipase activity may play an important role in H. pylori-associated gastric epithelial cell damage.…”

Section: Discussionmentioning

confidence: 97%

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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“…Bacterial load was found to be closely related with ulcer perforation in a group of patients undergoing surgical intervention due to ulcer disease [22]. Heavy bacterial loads indicated an increased frequency of bleeding in duodenal ulcer [23]. Significant correlation between bacterial count and acute as well as chronic inflammation has been repeatedly observed in numerous studies [24][25][26][27].…”

Section: Discussionmentioning

confidence: 99%

What is the impact of Helicobacter pylori density on the success of eradication therapy: A clinico-histopathological study

Önal¹,

Gökcan²,

Benzer³

et al. 2013

Clinics and Research in Hepatology and Gastroenterology

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Gastric mucosal hydrophobicity in duodenal ulceration: Role of Helicobacter pylori infection density and mucus lipids

Cited by 33 publications

References 1 publication

Age and Helicobacter pylori decrease gastric mucosal surface hydrophobicity independently

Age and Helicobacter pylori decrease gastric mucosal surface hydrophobicity independently

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

What is the impact of Helicobacter pylori density on the success of eradication therapy: A clinico-histopathological study

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