Alteration in the composition of cholesteryl glucosides and other lipids in undergoing morphological change from spiral to coccoid form

Shimomura, Hirofumi; Hayashi, Shunji; Yokota, Kenji; Oguma, Keiji; Hirai, Yoshikazu

doi:10.1016/j.femsle.2004.07.004

Cited by 14 publications

(14 citation statements)

References 40 publications

(31 reference statements)

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“…Hence, VDP2 has a low binding affinity to both DPPE vesicles and DMPE vesicles. Given that PE is the most predominant glycerophospholipid in the cell membrane lipid compositions of H. pylori 14 , and given that DMPE is one of the most prevalent PE molecular species of this bacterium 6 , we can assume that VDP1 at least binds to the PE carrying two myristic acid molecules on the H. pylori cells. Based on the results shown in Fig.…”

Section: Resultsmentioning

confidence: 99%

“…H. pylori transforms morphologically from a helical shape to a coccoid shape when exposed to an anaerobic atmosphere 14 . When H. pylori altered to the coccoid shape is returned to a microaerophilic condition, the bacterium is incapable of recovering its helical shape or of forming colonies on an agar plate by a conventional culture procedure.…”

Section: Resultsmentioning

confidence: 99%

See 1 more Smart Citation

Identification and characterization of a vitamin D3 decomposition product bactericidal against Helicobacter pylori

Hosoda

Shimomura

Wanibuchi

et al. 2015

Sci Rep

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This study demonstrated that the vitamin D3 decomposition product VDP1 exerts an antibacterial action against Helicobacter pylori but not against other bacteria. Treatment with VDP1 induced a collapse of cell membrane structures of H. pylori and ultimately lysed the bacterial cells. A unique dimyristoyl phosphatidylethanolamine in the membrane lipid compositions contributed to the interaction of VDP1 with H. pylori cells. In separate experiments, VDP1 had no influence on the viability of the human cancer cell lines MKN45 and T47D and lacked any vitamin D3-like hormonal action against the latter. In both 1H and 13C NMR analyses, the spectra patterns of VDP1 corresponded with those of Grundmann's ketone. These results suggest that VDP1 (or Grundmann's ketone-type indene compound) may become a fundamental structure for the development of new antibacterial substances with selective bactericidal action against H. pylori.

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Identification and characterization of a vitamin D3 decomposition product bactericidal against Helicobacter pylori

Hosoda

Shimomura

Wanibuchi

et al. 2015

Sci Rep

View full text Add to dashboard Cite

show abstract

“…Hence, CdrA is unlikely to have a major role, if any, in coccoid formation. It is known, however, that the lipid composition of H. pylori changes substantially during the transition into coccoid forms [ 25 ].…”

Section: Introductionmentioning

confidence: 99%

Role of AmiA in the Morphological Transition of Helicobacter pylori and in Immune Escape

et al. 2006

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The human gastric pathogen Helicobacter pylori is responsible for peptic ulcers and neoplasia. Both in vitro and in the human stomach it can be found in two forms, the bacillary and coccoid forms. The molecular mechanisms of the morphological transition between these two forms and the role of coccoids remain largely unknown. The peptidoglycan (PG) layer is a major determinant of bacterial cell shape, and therefore we studied H. pylori PG structure during the morphological transition. The transition correlated with an accumulation of the N-acetyl-D-glucosaminyl-β(1,4)-N-acetylmuramyl-L-Ala–D-Glu (GM-dipeptide) motif. We investigated the molecular mechanisms responsible for the GM-dipeptide motif accumulation, and studied the role of various putative PG hydrolases in this process. Interestingly, a mutant strain with a mutation in the amiA gene, encoding a putative PG hydrolase, was impaired in accumulating the GM-dipeptide motif and transforming into coccoids. We investigated the role of the morphological transition and the PG modification in the biology of H. pylori. PG modification and transformation of H. pylori was accompanied by an escape from detection by human Nod1 and the absence of NF-κB activation in epithelial cells. Accordingly, coccoids were unable to induce IL-8 secretion by AGS gastric epithelial cells. amiA is, to our knowledge, the first genetic determinant discovered to be required for this morphological transition into the coccoid forms, and therefore contributes to modulation of the host response and participates in the chronicity of H. pylori infection.

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“…Electron microscopic analysis showed that some αCgT Δ H. pylori exhibited an aberrant coccoid form [36], [37] (Figure 3C). These results indicate that cholesteryl α-glucosides are critical for H. pylori growth and normal morphology.…”

Section: Resultsmentioning

confidence: 99%

Helicobacter pylori Cholesteryl α-Glucosides Contribute to Its Pathogenicity and Immune Response by Natural Killer T Cells

et al. 2013

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Approximately 10–15% of individuals infected with Helicobacter pylori will develop ulcer disease (gastric or duodenal ulcer), while most people infected with H. pylori will be asymptomatic. The majority of infected individuals remain asymptomatic partly due to the inhibition of synthesis of cholesteryl α-glucosides in H. pylori cell wall by α1,4-GlcNAc-capped mucin O-glycans, which are expressed in the deeper portion of gastric mucosa. However, it has not been determined how cholesteryl α-glucosyltransferase (αCgT), which forms cholesteryl α-glucosides, functions in the pathogenesis of H. pylori infection. Here, we show that the activity of αCgT from H. pylori clinical isolates is highly correlated with the degree of gastric atrophy. We investigated the role of cholesteryl α-glucosides in various aspects of the immune response. Phagocytosis and activation of dendritic cells were observed at similar degrees in the presence of wild-type H. pylori or variants harboring mutant forms of αCgT showing a range of enzymatic activity. However, cholesteryl α-glucosides were recognized by invariant natural killer T (iNKT) cells, eliciting an immune response in vitro and in vivo. Following inoculation of H. pylori harboring highly active αCgT into iNKT cell-deficient (Jα18−/−) or wild-type mice, bacterial recovery significantly increased in Jα18−/− compared to wild-type mice. Moreover, cytokine production characteristic of Th1 and Th2 cells dramatically decreased in Jα18−/− compared to wild-type mice. These findings demonstrate that cholesteryl α-glucosides play critical roles in H. pylori-mediated gastric inflammation and precancerous atrophic gastritis.

show abstract

Alteration in the composition of cholesteryl glucosides and other lipids in undergoing morphological change from spiral to coccoid form

Cited by 14 publications

References 40 publications

Identification and characterization of a vitamin D3 decomposition product bactericidal against Helicobacter pylori

Identification and characterization of a vitamin D3 decomposition product bactericidal against Helicobacter pylori

Role of AmiA in the Morphological Transition of Helicobacter pylori and in Immune Escape

Helicobacter pylori Cholesteryl α-Glucosides Contribute to Its Pathogenicity and Immune Response by Natural Killer T Cells

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