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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.

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.

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mRNA expression level of gastrin in the fundus of the stomach. Gastrin mRNA expression level in the stomach was examined by quantitative RT-PCR. Shown is the expression level in the fundus. Data are presented as the fold change in gene expression normalized to 3 reference genes and relative to the negative control group which is considered as 1. Data are shown as means + standard deviation. Significant differences in expression level between inoculated groups and negative control group are indicated by * p ≤ 0.05 (Mann-Whitney U test).
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Figure 6: mRNA expression level of gastrin in the fundus of the stomach. Gastrin mRNA expression level in the stomach was examined by quantitative RT-PCR. Shown is the expression level in the fundus. Data are presented as the fold change in gene expression normalized to 3 reference genes and relative to the negative control group which is considered as 1. Data are shown as means + standard deviation. Significant differences in expression level between inoculated groups and negative control group are indicated by * p ≤ 0.05 (Mann-Whitney U test).

Mentions: The peptide hormone gastrin stimulates the secretion of gastric acid by parietal cells. A disturbance in its expression may lead to hypergastrinemia. The expression of gastrin was highly up-regulated in the fundus of gerbils infected with ASB2 and ASB6 at 9 weeks post-infection (Figure 6 and Table 2). Compared to control animals, the mean relative expression was 6.79 ± 2.49 for ASB2- and 10.35 ± 2.39 for ASB6-infected gerbils. In the antrum of the stomach, no up-regulation of gastrin expression was detected.


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)

mRNA expression level of gastrin in the fundus of the stomach. Gastrin mRNA expression level in the stomach was examined by quantitative RT-PCR. Shown is the expression level in the fundus. Data are presented as the fold change in gene expression normalized to 3 reference genes and relative to the negative control group which is considered as 1. Data are shown as means + standard deviation. Significant differences in expression level between inoculated groups and negative control group are indicated by * p ≤ 0.05 (Mann-Whitney U test).
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Figure 6: mRNA expression level of gastrin in the fundus of the stomach. Gastrin mRNA expression level in the stomach was examined by quantitative RT-PCR. Shown is the expression level in the fundus. Data are presented as the fold change in gene expression normalized to 3 reference genes and relative to the negative control group which is considered as 1. Data are shown as means + standard deviation. Significant differences in expression level between inoculated groups and negative control group are indicated by * p ≤ 0.05 (Mann-Whitney U test).
Mentions: The peptide hormone gastrin stimulates the secretion of gastric acid by parietal cells. A disturbance in its expression may lead to hypergastrinemia. The expression of gastrin was highly up-regulated in the fundus of gerbils infected with ASB2 and ASB6 at 9 weeks post-infection (Figure 6 and Table 2). Compared to control animals, the mean relative expression was 6.79 ± 2.49 for ASB2- and 10.35 ± 2.39 for ASB6-infected gerbils. In the antrum of the stomach, no up-regulation of gastrin expression was detected.

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