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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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H&E staining of the antrum of a gerbil stomach. Normal histology of the antrum of a sham-inoculated negative control animal (a). Explicit lymphocytic infiltration of the lamina propria and the submucosa with the formation of lymphoid follicles (arrows) in the antrum of a gerbil inoculated with H. heilmannii s.s. ASB1 (b). Mild to absent lymphocytic infiltration (arrows) of the lamina propria in the antrum of a gerbil inoculated with H. heilmannii s.s. ASB7 (c). Bar = 30 μm.
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Figure 1: H&E staining of the antrum of a gerbil stomach. Normal histology of the antrum of a sham-inoculated negative control animal (a). Explicit lymphocytic infiltration of the lamina propria and the submucosa with the formation of lymphoid follicles (arrows) in the antrum of a gerbil inoculated with H. heilmannii s.s. ASB1 (b). Mild to absent lymphocytic infiltration (arrows) of the lamina propria in the antrum of a gerbil inoculated with H. heilmannii s.s. ASB7 (c). Bar = 30 μm.

Mentions: The stomach of all control animals showed a normal histomorphology (Figure 1a). Inflammation in the stomach of gerbils infected with H. heilmannii s.s. strains ASB1, ASB2, ASB3, ASB6, ASB11, ASB13 and ASB14 was marked by a chronic active gastritis with formation of lymphocytic aggregates in the lamina propria and submucosa of the antrum of the stomach (Figure 1b). The mucosal thickness was slightly increased and only few neutrophils were detected. In contrast, H. heilmannii s.s. strains ASB7 and ASB9 did not cause explicit antral inflammation and only a mild increase in lymphocytic cell number was observed in the lamina propria of the antrum of the stomach (Figure 1c). In all H. heilmannii s.s.-infected gerbils, only limited signs of inflammation were detected in the fundus of the stomach (Additional file 1). The antral inflammation scores of each individual animal are shown in Figure 2d. A statistically significant difference between inflammation scores for gerbils inoculated with ASB1, ASB2, ASB3, ASB6, ASB11, ASB13 and ASB14 compared with the control group was demonstrated (Mann-Whitney U test, p < 0.05, Figure 2d).


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)

H&E staining of the antrum of a gerbil stomach. Normal histology of the antrum of a sham-inoculated negative control animal (a). Explicit lymphocytic infiltration of the lamina propria and the submucosa with the formation of lymphoid follicles (arrows) in the antrum of a gerbil inoculated with H. heilmannii s.s. ASB1 (b). Mild to absent lymphocytic infiltration (arrows) of the lamina propria in the antrum of a gerbil inoculated with H. heilmannii s.s. ASB7 (c). Bar = 30 μm.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Figure 1: H&E staining of the antrum of a gerbil stomach. Normal histology of the antrum of a sham-inoculated negative control animal (a). Explicit lymphocytic infiltration of the lamina propria and the submucosa with the formation of lymphoid follicles (arrows) in the antrum of a gerbil inoculated with H. heilmannii s.s. ASB1 (b). Mild to absent lymphocytic infiltration (arrows) of the lamina propria in the antrum of a gerbil inoculated with H. heilmannii s.s. ASB7 (c). Bar = 30 μm.
Mentions: The stomach of all control animals showed a normal histomorphology (Figure 1a). Inflammation in the stomach of gerbils infected with H. heilmannii s.s. strains ASB1, ASB2, ASB3, ASB6, ASB11, ASB13 and ASB14 was marked by a chronic active gastritis with formation of lymphocytic aggregates in the lamina propria and submucosa of the antrum of the stomach (Figure 1b). The mucosal thickness was slightly increased and only few neutrophils were detected. In contrast, H. heilmannii s.s. strains ASB7 and ASB9 did not cause explicit antral inflammation and only a mild increase in lymphocytic cell number was observed in the lamina propria of the antrum of the stomach (Figure 1c). In all H. heilmannii s.s.-infected gerbils, only limited signs of inflammation were detected in the fundus of the stomach (Additional file 1). The antral inflammation scores of each individual animal are shown in Figure 2d. A statistically significant difference between inflammation scores for gerbils inoculated with ASB1, ASB2, ASB3, ASB6, ASB11, ASB13 and ASB14 compared with the control group was demonstrated (Mann-Whitney U test, p < 0.05, Figure 2d).

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