Virulence Factors of Helicobacter pylori — Ultrastructural Features

Bode, Günter; Malfertheiner, Peter; Lehnhardt, G.; Ditschuneit, H.

doi:10.1007/978-3-642-75315-2_10

Cited by 16 publications

(9 citation statements)

References 33 publications

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“…H. pylori with these atypical structures is seen occasionally in vivo (Caselli et al, 1993 ;Chan et al, 1994 ;Janas et al, 1995 ;Noach et al, 1994), but most frequently in vitro in old cultures (Andersen et al, 1997 ;Catrenich & Makin, 1991 ;Cellini et al, 1994 ;Jones & Curry, 1990 ;Kusters et al, 1997 ;Mai et al, 1989 ;Moshkowitz et al, 1994 ;Nilius et al, 1993). It remains uncertain whether coccoidal forms are degenerative (Buck et al, 1986 ;Catrenich & Makin, 1991 ;Cellini et al, 1994 ;Kusters et al, 1997 ;Nilius et al, 1993), or adaptations to marginal or hostile environments (Janas et al, 1995), with a capacity for transmission and regrowth to the bacillary form (Andersen et al, 1997 ;Benaissa et al, 1996 ;Bode et al, 1991 ;Jones & Curry, 1990 ;Mai et al, 1989).…”

Section: Introductionmentioning

confidence: 99%

The relationship between Helicobacter pylori motility, morphology and phase of growth: implications for gastric colonization and pathology

et al. 1999

Microbiology

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To explore the relationship between Helicobacter pylori motility, morphology and phase of growth, bacteria were isolated from antral biopsies of patients with duodenal ulcer or non-ulcer dyspepsia, and grown in liquid medium in batch and continuous culture systems. Motilities and morphologies of H. pylori in different phases of growth were examined with a Hobson BackTracker and by transmission electron microscopy. Morphologies of bacteria grown in vitro were also compared with those of bacteria in antral biopsies from patients with non-autoimmune gastritis. H. pylori had poor motility in lag phase, became highly motile in mid-exponential phase and lost motility in the decline phase of growth. Motilities of bacteria in the same phase of growth from patients with duodenal ulcer or non-ulcer dyspepsia were not significantly different. In the mid/late-exponential phase of growth bacteria had helical morphologies and multiple polar flagella, typical of H. pylori in the gastric mucus layer. In the decline phase of growth bacteria shed flagella, and had precoccoidal or coccoidal morphologies. These findings support the view that helical and coccoidal H. pylori are in different phases of growth with different roles in gastric colonization, indicate that bacterial motility per se is unlikely to be a determinant of H. pylori pathology, and suggest that H. pylori in the antral mucus layer is in a state of continuous (exponential phase) growth.

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Section: Introductionmentioning

confidence: 99%

The relationship between Helicobacter pylori motility, morphology and phase of growth: implications for gastric colonization and pathology

et al. 1999

Microbiology

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“…It has been reported that urease, protease, phospholipase A2, and vacuolating toxin are virulence factors of H. pylori (3). In particular, ammonia produced from urea by the action of urease enables H. pylori to survive in gastric acid by neutralization of hydrogen ions around the organisms (20) and injures gastric mucosal epithelial cells (3,20,29). It has been shown that ammonia may affect the mucosal charge gradient, paracellular permeability, and epithelial cell Na ϩ /K ϩ ATPase, leading to back diffusion of hydrogen ions and resulting in gastric ulcer formation (10).…”

mentioning

confidence: 99%

Bacterial activity of a new antiulcer agent, ecabet sodium, against Helicobacter pylori under acidic conditions

Shibata

Ito

Hongo

et al. 1995

Antimicrob Agents Chemother

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Helicobacter pylori NCTC 11637, which is nonviable at pH 3.0, became viable after addition of 10 mM urea owing to ammonia production by urease. In a buffer supplemented with urea, ecabet sodium decreased both the production of ammonia and the number of viable cells of H. pylori NCTC 11637 and changed the bacteria from the bacilliform to the horseshoe or doughnut shape in a concentration-dependent manner. In particular, ecabet sodium (2 and 4 mg/ml) decreased the number of viable cells below the control level. Benzohydroxamic acid, a urease inhibitor, also caused a decrease in ammonia production accompanied by a decrease in the number of viable cells and changed the morphological form at pH 3.0, but the number of viable cells was not lowered below the control level. In buffers at various pHs without urea, ecabet sodium showed a concentrationdependent bactericidal effect on H. pylori at pHs 4.0 and 5.0 but not at pHs 6.0 and 7.0 while benzohydroxamic acid caused only a slight decrease in the number of viable cells at pH 4.0. These results suggest that ecabet sodium has strong bactericidal activity in addition to its urease-inhibiting activity under acidic conditions.

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“… 28 In the present study, the pepsin treatment partly degraded the native glycoprotein into the lower molecular weight form, which was intermediate in size between the subunit and the native glycoprotein. The scanning electron microscopic study, however, revealed that the three‐dimensional network‐like ultrastructure of the adherent mucus, which is a stable and protective form of the mucus layer, 9 was disrupted by the pepsin treatment into a fragile form of lumpy globular appearance. Furthermore, in the light microscopic observation, pepsin caused the disruption of the adherent mucus layer and an extensive degeneration of epithelial cells.…”

Section: Discussionmentioning

confidence: 99%

“…35 Colonization of H. pylori signi®cantly decreased the gel-forming polymeric mucin content in adherent mucus, and altered the threedimensional network ultrastructure of the gastric mucus gel layer, giving it a fragile, lumpy, globular appearance. 9,36 Further, some experimental studies using rat 7,37 and pig 8 also demonstrated that the proportion of degraded and lower molecular weight glycoprotein in the mucus gel layer increased in injured stomachs caused by aspirin or bile duct ligation. Accordingly, the mucus glycoprotein in ulcerated or H. pylori-positive stomachs is less able to provide protection against acid, pepsin and other ulcerative stimuli.…”

Section: Discussionmentioning

confidence: 99%

“…Degraded and lower molecular weight gastric mucins lose both their viscosity and their barrier function 6 . Various noxious factors such as NSAIDs, bile acids and Helicobacter pylori ‐derived protease and urease reduce the integrity of the gastric mucus gel layer 7 –9 . Maintenance of the polymeric structure of gastric mucus glycoproteins and gastric mucus secretion is therefore essential for gastroprotection.…”

Section: Introductionmentioning

confidence: 99%

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Ecabet sodium, a novel locally‐acting anti‐ulcer agent, protects the integrity of the gastric mucosal gel layer from pepsin‐induced disruption in the rat

Kinoshita¹,

Endo²,

Yasoshima³

et al. 1999

Aliment Pharmacol Ther

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Background : Ecabet sodium, a novel non‐systemic anti‐ulcer agent, possesses high affinity to gastric adherent mucus, which plays an important role in the protection of the gastric epithelium against acid and pepsin. Aim : To assess the effect of ecabet on pepsin‐induced degradation of the structure of the mucus gel layer. Methods : Everted sacs of rat stomach were incubated in HCl solution containing pepsin with or without ecabet. Pepsin‐induced release of the cleaved peptides and hexosamine from the sacs was determined. Changes in the molecular size of glycoproteins in the adherent mucus (using gel filtration methods) and in the morphology of the epithelium (using both light and scanning electron microscopy) were also examined. Results : Ecabet reduced the pepsin‐induced release of peptides and hexosamine, depending on its content in the adherent mucus. Pepsin treatment partially lowered the molecular weight of native glycoproteins in the adherent mucus, caused exfoliation of the epithelial cells, and degraded the network‐like ultrastructure of the mucus layer, giving it a lumpy, globular appearance. Ecabet prevented both the pepsin‐induced molecular size shift in mucus glycoproteins, and morphological alteration of the epithelium, including ultrastructural derangement of the mucus gel layer. Conclusion : Ecabet protects the polymeric structure of mucus glycoproteins from proteolytic degradation by pepsin, and thus maintains integrity of the gastric mucus gel layer.

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Virulence Factors of Helicobacter pylori — Ultrastructural Features

Cited by 16 publications

References 33 publications

The relationship between Helicobacter pylori motility, morphology and phase of growth: implications for gastric colonization and pathology

The relationship between Helicobacter pylori motility, morphology and phase of growth: implications for gastric colonization and pathology

Bacterial activity of a new antiulcer agent, ecabet sodium, against Helicobacter pylori under acidic conditions

Ecabet sodium, a novel locally‐acting anti‐ulcer agent, protects the integrity of the gastric mucosal gel layer from pepsin‐induced disruption in the rat

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