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Diversity in bacterium-host interactions within the species Helicobacter heilmannii sensu stricto.

Joosten M, Blaecher C, Flahou B, Ducatelle R, Haesebrouck F, Smet A - Vet. Res. (2013)

Bottom Line: A reduced antral expression of H+/K+ ATPase was seen in the stomach after infection with 3 highly colonizing strains and 2 highly colonizing strains caused an increased gastrin expression in the fundus.In none of the H. heilmannii s.s.-infected groups, IFN-γ expression was up-regulated.This study demonstrates diversity in bacterium-host interactions within the species H. heilmannii s.s. and that the pathogenesis of gastric infections with this microorganism is not identical to that of an H. pylori infection.

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ABSTRACT
Helicobacter (H.) heilmannii sensu stricto (s.s.) is a zoonotic bacterium that naturally colonizes the stomach of dogs and cats. In humans, this microorganism has been associated with gastritis, peptic ulcer disease and mucosa associated lymphoid tissue (MALT) lymphoma. Little information is available about the pathogenesis of H. heilmannii s.s. infections in humans and it is unknown whether differences in virulence exist within this species. Therefore, a Mongolian gerbil model was used to study bacterium-host interactions of 9 H. heilmannii s.s. strains. The colonization ability of the strains, the intensity of gastritis and gene expression of various inflammatory cytokines in the stomach were determined at 9 weeks after experimental infection. The induction of an antrum-dominant chronic active gastritis with formation of lymphocytic aggregates was shown for 7 strains. High-level antral colonization was seen for 4 strains, while colonization of 4 other strains was more restricted and one strain was not detected in the stomach at 9 weeks post infection. All strains inducing a chronic active gastritis caused an up-regulation of the pro-inflammatory cytokine IL-1β in the antrum. A reduced antral expression of H+/K+ ATPase was seen in the stomach after infection with 3 highly colonizing strains and 2 highly colonizing strains caused an increased gastrin expression in the fundus. In none of the H. heilmannii s.s.-infected groups, IFN-γ expression was up-regulated. This study demonstrates diversity in bacterium-host interactions within the species H. heilmannii s.s. and that the pathogenesis of gastric infections with this microorganism is not identical to that of an H. pylori infection.

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Gastric antral epithelial cell proliferation. Ki67 staining of the antrum of a gerbil inoculated with H. heilmannii s.s. ASB1 (b) showing a higher number of proliferating epithelial cells compared to a sham-inoculated negative control animal (a). The rate of epithelial cell proliferation was determined by counting Ki67-positive epithelial cells in 5 randomly chosen High Power Fields at the level of the gastric pits (magnification: 400×) in the antrum of the gerbil stomach (c). The mean numbers of Ki67-positive cells are shown in each experimental group. Significant differences between H. heilmannii s.s.-inoculated and control animals are indicated by * (ANOVA, p < 0.05). Significant differences in comparison with ASB7 and ASB9 inoculated groups are indicated by + and # respectively (ANOVA, p < 0.05).
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Figure 3: Gastric antral epithelial cell proliferation. Ki67 staining of the antrum of a gerbil inoculated with H. heilmannii s.s. ASB1 (b) showing a higher number of proliferating epithelial cells compared to a sham-inoculated negative control animal (a). The rate of epithelial cell proliferation was determined by counting Ki67-positive epithelial cells in 5 randomly chosen High Power Fields at the level of the gastric pits (magnification: 400×) in the antrum of the gerbil stomach (c). The mean numbers of Ki67-positive cells are shown in each experimental group. Significant differences between H. heilmannii s.s.-inoculated and control animals are indicated by * (ANOVA, p < 0.05). Significant differences in comparison with ASB7 and ASB9 inoculated groups are indicated by + and # respectively (ANOVA, p < 0.05).

Mentions: Results of the gastric epithelial cell proliferation scoring in the antrum of the stomach are shown in Figure 3c. Significantly higher numbers of Ki67-positive proliferating epithelial cells were seen in the antrum of ASB1- and ASB6-infected gerbils, compared to the control group (ANOVA, p < 0.05, Figure 3a-b). Numbers of Ki67-positive cells were moderately increased in ASB2-, ASB3-, ASB11-, ASB13- and ASB14-infected gerbils, although not statistically significant. H. heilmannii s.s. strains ASB7 and ASB9 did not cause an increase of gastric epithelial cell proliferation. In addition, significantly higher numbers of proliferating epithelial cells were demonstrated in the antrum of ASB1-, ASB2-, and ASB6-infected gerbils, compared to gerbils infected with ASB7 and ASB9 (ANOVA, p < 0.05).


Diversity in bacterium-host interactions within the species Helicobacter heilmannii sensu stricto.

Joosten M, Blaecher C, Flahou B, Ducatelle R, Haesebrouck F, Smet A - Vet. Res. (2013)

Gastric antral epithelial cell proliferation. Ki67 staining of the antrum of a gerbil inoculated with H. heilmannii s.s. ASB1 (b) showing a higher number of proliferating epithelial cells compared to a sham-inoculated negative control animal (a). The rate of epithelial cell proliferation was determined by counting Ki67-positive epithelial cells in 5 randomly chosen High Power Fields at the level of the gastric pits (magnification: 400×) in the antrum of the gerbil stomach (c). The mean numbers of Ki67-positive cells are shown in each experimental group. Significant differences between H. heilmannii s.s.-inoculated and control animals are indicated by * (ANOVA, p < 0.05). Significant differences in comparison with ASB7 and ASB9 inoculated groups are indicated by + and # respectively (ANOVA, p < 0.05).
© Copyright Policy - open-access
Related In: Results  -  Collection

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Show All Figures
getmorefigures.php?uid=PMC3750284&req=5

Figure 3: Gastric antral epithelial cell proliferation. Ki67 staining of the antrum of a gerbil inoculated with H. heilmannii s.s. ASB1 (b) showing a higher number of proliferating epithelial cells compared to a sham-inoculated negative control animal (a). The rate of epithelial cell proliferation was determined by counting Ki67-positive epithelial cells in 5 randomly chosen High Power Fields at the level of the gastric pits (magnification: 400×) in the antrum of the gerbil stomach (c). The mean numbers of Ki67-positive cells are shown in each experimental group. Significant differences between H. heilmannii s.s.-inoculated and control animals are indicated by * (ANOVA, p < 0.05). Significant differences in comparison with ASB7 and ASB9 inoculated groups are indicated by + and # respectively (ANOVA, p < 0.05).
Mentions: Results of the gastric epithelial cell proliferation scoring in the antrum of the stomach are shown in Figure 3c. Significantly higher numbers of Ki67-positive proliferating epithelial cells were seen in the antrum of ASB1- and ASB6-infected gerbils, compared to the control group (ANOVA, p < 0.05, Figure 3a-b). Numbers of Ki67-positive cells were moderately increased in ASB2-, ASB3-, ASB11-, ASB13- and ASB14-infected gerbils, although not statistically significant. H. heilmannii s.s. strains ASB7 and ASB9 did not cause an increase of gastric epithelial cell proliferation. In addition, significantly higher numbers of proliferating epithelial cells were demonstrated in the antrum of ASB1-, ASB2-, and ASB6-infected gerbils, compared to gerbils infected with ASB7 and ASB9 (ANOVA, p < 0.05).

Bottom Line: A reduced antral expression of H+/K+ ATPase was seen in the stomach after infection with 3 highly colonizing strains and 2 highly colonizing strains caused an increased gastrin expression in the fundus.In none of the H. heilmannii s.s.-infected groups, IFN-γ expression was up-regulated.This study demonstrates diversity in bacterium-host interactions within the species H. heilmannii s.s. and that the pathogenesis of gastric infections with this microorganism is not identical to that of an H. pylori infection.

View Article: PubMed Central - HTML - PubMed

ABSTRACT
Helicobacter (H.) heilmannii sensu stricto (s.s.) is a zoonotic bacterium that naturally colonizes the stomach of dogs and cats. In humans, this microorganism has been associated with gastritis, peptic ulcer disease and mucosa associated lymphoid tissue (MALT) lymphoma. Little information is available about the pathogenesis of H. heilmannii s.s. infections in humans and it is unknown whether differences in virulence exist within this species. Therefore, a Mongolian gerbil model was used to study bacterium-host interactions of 9 H. heilmannii s.s. strains. The colonization ability of the strains, the intensity of gastritis and gene expression of various inflammatory cytokines in the stomach were determined at 9 weeks after experimental infection. The induction of an antrum-dominant chronic active gastritis with formation of lymphocytic aggregates was shown for 7 strains. High-level antral colonization was seen for 4 strains, while colonization of 4 other strains was more restricted and one strain was not detected in the stomach at 9 weeks post infection. All strains inducing a chronic active gastritis caused an up-regulation of the pro-inflammatory cytokine IL-1β in the antrum. A reduced antral expression of H+/K+ ATPase was seen in the stomach after infection with 3 highly colonizing strains and 2 highly colonizing strains caused an increased gastrin expression in the fundus. In none of the H. heilmannii s.s.-infected groups, IFN-γ expression was up-regulated. This study demonstrates diversity in bacterium-host interactions within the species H. heilmannii s.s. and that the pathogenesis of gastric infections with this microorganism is not identical to that of an H. pylori infection.

Show MeSH
Related in: MedlinePlus