<i>In Vitro</i> Aging of <i>Helicobacter pylori</i>: Changes in Morphology, Intracellular Composition and Surface Properties

Enroth, Helena; Wreiber, Karin; Rigo, R.; Risberg, Dag; Uribe, A.; Engstrand, Lars

doi:10.1046/j.1523-5378.1999.09034.x

Cited by 36 publications

(34 citation statements)

References 35 publications

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“…Different chemicals as bismuth, as well as bile acids, antibiotics, temperature, nutritients, oxygen tension, starvation and aging are some examples [3,10,15,16,21,25].…”

Section: Resultsmentioning

confidence: 99%

“…The role of the coccoid form in pathogenesis of H. pylori-associated gastritis has been disputed. Some authors consider the coccoid form as a degenerative or dead form of H. pylori [ 16,21,25], while others consider it as a resting but still metabolic active form [2, 3,12,22,29,321. The aim of this study was to demonstrate the conversion of spiral form of H. pylon to coccoid forms, and to show both degenerative and intact subcellar morphology suggesting that some of the coccoid bacteria may be viable.…”

Section: Introductionmentioning

confidence: 99%

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Morphologic Conversion of Helicobacter Pylori from Spiral to Coccoid Form: Scanning (SEM) and Transmission Electron Microscopy (TEM) Suggest Viability

Wïllén¹,

Carlén²,

Wang³

et al. 2000

Upsala Journal of Medical Sciences

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Helicobacter pylon is a pathogen associated with type B gastritis, peptic ulcer disease, gastric atrophy, and stomach cancer. H. pylori exists in two morphological forms, spirals and coccoids. The latter has been described as viable but non-cultivable. The role of the coccoid form in the pathogenesis of gastric disease is disputed. Some authors consider the coccoid form to be a degenerative or dead form of H.pylori, while others consider it a resting but still metabolically active form.This study reports the conversion fiom spiral to coccoid form ultrastructurally. Dense material is accumulated in the periplasmic space, the spiral bacteria bend and the outer membrane is separated from the inner cell wall layer. Remodeling of inner structures takes place, ending in the coccoid form of the bacteria with preserved light polyphosphate areas. Reduction of surface takes place by production of surface membrane vesicles, which later are squeezed off. The finding of preserved subcellular structures +d intact double membranes in combination with degenerative forms suggests that some of the coccoids are viable. Scanning electron microscopy (SEM) demonstrates coccoid form of bacteria with slightly ruffled surfaces but no spiral forms.

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“…Different chemicals as bismuth, as well as bile acids, antibiotics, temperature, nutritients, oxygen tension, starvation and aging are some examples [3,10,15,16,21,25].…”

Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Morphologic Conversion of Helicobacter Pylori from Spiral to Coccoid Form: Scanning (SEM) and Transmission Electron Microscopy (TEM) Suggest Viability

Wïllén¹,

Carlén²,

Wang³

et al. 2000

Upsala Journal of Medical Sciences

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“…Although usually spiral-shaped, the bacterium can appear as a rod, while coccoid shapes appear after prolonged in vitro culture or antibiotic treatment (342). These coccoids cannot be cultured in vitro and are thought to represent dead cells (342), although it has been suggested that coccoid forms may represent a viable, nonculturable state (162). The organism has 2 to 6 unipolar, sheathed flagella of approximately 3 m in length, which often carry a distinctive bulb at the end (481).…”

Section: Microbiology Of H Pylorimentioning

confidence: 99%

Pathogenesis ofHelicobacter pyloriInfection

2006

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SUMMARY Helicobacter pylori is the first formally recognized bacterial carcinogen and is one of the most successful human pathogens, as over half of the world's population is colonized with this gram-negative bacterium. Unless treated, colonization usually persists lifelong. H. pylori infection represents a key factor in the etiology of various gastrointestinal diseases, ranging from chronic active gastritis without clinical symptoms to peptic ulceration, gastric adenocarcinoma, and gastric mucosa-associated lymphoid tissue lymphoma. Disease outcome is the result of the complex interplay between the host and the bacterium. Host immune gene polymorphisms and gastric acid secretion largely determine the bacterium's ability to colonize a specific gastric niche. Bacterial virulence factors such as the cytotoxin-associated gene pathogenicity island-encoded protein CagA and the vacuolating cytotoxin VacA aid in this colonization of the gastric mucosa and subsequently seem to modulate the host's immune system. This review focuses on the microbiological, clinical, immunological, and biochemical aspects of the pathogenesis of H. pylori.

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“…Lactose again prevented the bactericidal effect of Gal3. H. pylori bacteria are also known to change shape from spiral to coccoid under unfavorable conditions (35). As shown in Fig.…”

Section: Cd3mentioning

confidence: 99%

Galectin-3 Plays an Important Role in Innate Immunity to Gastric Infection by Helicobacter pylori

et al. 2016

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We studied the role of galectin-3 (Gal3) in gastric infection by Helicobacter pylori. We first demonstrated that Gal3 was selectively expressed by gastric surface epithelial cells and abundantly secreted into the surface mucus layer. We next inoculated H. pylori Sydney strain 1 into wild-type (WT) and Gal3-deficient mice using a stomach tube. At 2 weeks postinoculation, the bacterial cells were mostly trapped within the surface mucus layer in WT mice. In sharp contrast, they infiltrated deep into the gastric glands in Gal3-deficient mice. Bacterial loads in the gastric tissues were also much higher in Gal3-deficient mice than in WT mice. At 6 months postinoculation, H. pylori had successfully colonized within the gastric glands of both WT and Gal3-deficient mice, although the bacterial loads were still higher in the latter. Furthermore, large lymphoid clusters mostly consisting of B cells were frequently observed in the gastric submucosa of Gal3-deficient mice. In vitro, peritoneal macrophages from Gal3-deficient mice were inefficient in killing engulfed H. pylori. Furthermore, recombinant Gal3 not only induced rapid aggregation of H. pylori but also exerted a potent bactericidal effect on H. pylori as revealed by propidium iodide uptake and a morphological shift from spiral to coccoid form. However, a minor fraction of bacterial cells, probably transient phase variants of Gal3-binding sugar moieties, escaped killing by Gal3. Collectively, our data demonstrate that Gal3 plays an important role in innate immunity to infection and colonization of H. pylori.

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In Vitro Aging of Helicobacter pylori: Changes in Morphology, Intracellular Composition and Surface Properties

Cited by 36 publications

References 35 publications

Morphologic Conversion of Helicobacter Pylori from Spiral to Coccoid Form: Scanning (SEM) and Transmission Electron Microscopy (TEM) Suggest Viability

Morphologic Conversion of Helicobacter Pylori from Spiral to Coccoid Form: Scanning (SEM) and Transmission Electron Microscopy (TEM) Suggest Viability

Pathogenesis ofHelicobacter pyloriInfection

Galectin-3 Plays an Important Role in Innate Immunity to Gastric Infection by Helicobacter pylori

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