Virulence of Coccoid and Bacillary Forms of Helicobacter pylori in Gnotobiotic Piglets

Eaton, KA; Catrenich, Carl E.; Makin, Kelly M.; Krakowka, Steven

doi:10.1093/infdis/171.2.459

Cited by 88 publications

(60 citation statements)

References 9 publications

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“…Most of the H. pylori colonizing the gastric antrum are to be found within the mucus environment (Terada et al, 1993 ;Thomsen et al, 1990) and [as we and other investigators (Buck et al, 1986 ;Hazell et al, 1986 ;Megraud, 1989) have shown] invariably possess helical morphologies. This observation, in conjunction with results from our in vitro studies of bacterial motility and morphology, and the dependence of gastric colonization on bacterial motility (Eaton et al, 1989(Eaton et al, , 1992, lead us to conclude that the typical H. pylori population within the antral mucus layer is in a state of continuous (exponential phase) growth. To maintain a bacterial population in continuous growth the nutrient supply must at all times exceed that required by the bacteria (Duguid et al, 1978).…”

Section: Implications For Gastric Colonizationsupporting

confidence: 75%

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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: Implications For Gastric Colonizationsupporting

confidence: 75%

“…Bacterial motility is generally held to be a requirement for H. pylori colonization of the stomach (Eaton et al, 1989(Eaton et al, , 1992. Consistent with this view, the bacteria in vivo typically possess helical morphologies and multiple polar flagella (Hazell et al, 1986).…”

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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“…Huang et al [19] reported an IL-8-inducing activity in supernates from overnight culture of H. pylori, suggesting that the coccoid form produces less of this kind of activity. Furthermore, the induction of IL-8 secretion was different depending on both the H. pylori strains used and the epithelial cells used [20]. In this study, strain diversity in terms of the stimulating activity of IL-8 secretion was demonstrated.…”

Section: Discussionmentioning

confidence: 72%

Interleukin-8 induction and adhesion of the coccoid form of Helicobacter pylori

Osaki¹,

Yamaguchi²,

Taguchi³

et al. 2002

Journal of Medical Microbiology

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To determine the pathological significance of the coccoid form of Helicobacter pylori, its adhesion to and induction of secretion of interleukin-8 (IL-8) by gastric epithelial (MKN45) cells were studied. By flow cytometry, the adhesion of the coccoid form to MKN45 cells was significantly lower than that of the helical form. The monoclonal antibody A20 recognising lipopolysaccharide of H. pylori inhibited the adhesion of the coccoid form to MKN45 cells as much as that of the helical form. There was significantly lower induction of IL-8 secretion by MKN45 cells exposed to the coccoid form (two of four strains) as compared with the helical form.

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“…The bacteria were confirmed to be H. pylori by Gram stain morphology and the presence of urease, oxidase, and catalase activity (see below) and stored at Ϫ70°C in Brucella broth plus sterile glycerol 20% v/v. To infect mice, low-passaged organisms were thawed, cultured for 72 to 96 h on Brucella agar, enumerated by nephelometry, and administered by gavage within 20 min of harvesting to prevent bacterial transition from infective spiral to noninfective coccoid forms (23,24).…”

Section: Bacteriamentioning

confidence: 99%

Helicobacter pylori-Induced Mucosal Inflammation Is Th1 Mediated and Exacerbated in IL-4, But Not IFN-γ, Gene-Deficient Mice

Smythies

Waites²,

Lindsey

et al. 2000

The Journal of Immunology

313

220

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To elucidate the pathogenesis of Helicobacter pylori-associated gastritis, we studied immune responses of C57BL/6J wild-type (WT), SCID, and gene deficient (IFN-γ−/− and IL-4−/−) mice following infection with a pathogenic isolate of H. pylori (SPM326). During early infection in WT mice, mononuclear and polymorphonuclear cells accumulated in the gastric lamina propria, and the numbers of cells in the inflamed mucosa expressing IFN-γ, but not IL-4, mRNA rose significantly (p < 0.005), consistent with a local Th1 response. Splenic T cells from the same infected WT mice produced high levels of IFN-γ, no detectable IL-4, and low amounts of IL-10 following in vitro H. pylori urease stimulation, reflecting a systemic Th1 response. Infected C57BL/6J SCID mice did not develop gastric inflammation despite colonization by many bacteria. Infected C57BL/10J and BALB/c mice also did not develop gastric inflammation and displayed a mixed Th1/Th2 splenic cytokine profile. These data imply a major role for the Th1 cytokine IFN-γ in H. pylori-associated gastric inflammation in C57BL/6J mice. Compared with WT animals, infected IL-4−/− animals had more severe gastritis and higher levels of IFN-γ production by urease-stimulated splenocytes (p < 0.01), whereas IFN-γ−/− mice exhibited no gastric inflammation and higher levels of IL-4 production by stimulated splenocytes. These findings establish C57BL/6J mice as an important model for H. pylori infection and demonstrate that up-regulated production of IFN-γ, in the absence of the opposing effects of IL-4 (and possibly IL-10), plays a pivotal role in promoting H. pylori-induced mucosal inflammation.

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Virulence of Coccoid and Bacillary Forms of Helicobacter pylori in Gnotobiotic Piglets

Cited by 88 publications

References 9 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

Interleukin-8 induction and adhesion of the coccoid form of Helicobacter pylori

Helicobacter pylori-Induced Mucosal Inflammation Is Th1 Mediated and Exacerbated in IL-4, But Not IFN-γ, Gene-Deficient Mice

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