| 1. |
- Flahou, Bram, et al.
(författare)
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Evidence for a primate origin of zoonotic Helicobacter suis colonizing domesticated pigs.
- 2018
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Ingår i: The ISME journal. - : Springer Science and Business Media LLC. - 1751-7370 .- 1751-7362. ; 12:1, s. 77-86
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Tidskriftsartikel (refereegranskat)abstract
- Helicobacter suis is the second most prevalent Helicobacter species in the stomach of humans suffering from gastric disease. This bacterium mainly inhabits the stomach of domesticated pigs, in which it causes gastric disease, but it appears to be absent in wild boars. Interestingly, it also colonizes the stomach of asymptomatic rhesus and cynomolgus monkeys. The origin of modern human-, pig- or non-human primate-associated H. suis strains in these respective host populations was hitherto unknown. Here we show that H. suis in pigs possibly originates from non-human primates. Our data suggest that a host jump from macaques to pigs happened between 100000 and 15000 years ago and that pig domestication has had a significant impact on the spread of H. suis in the pig population, from where this pathogen occasionally infects humans. Thus, in contrast to our expectations, H. suis appears to have evolved in its main host in a completely different way than its close relative Helicobacter pylori in humans.
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| 2. |
- Ohno, Tomoyuki, et al.
(författare)
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Effects of BabA expression during H. pylori infection of Mongolian gerbils
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Annan publikation (övrigt vetenskapligt/konstnärligt)abstract
- Objective: Helicobacter pylori outer membrane proteins, such as the BabA adhesin are associated with severe pathological outcome. However, the in vivo role of the BabA adhesin during long-term infection is not clear. Design and Setting: Mongolian gerbils were inoculated with the H. pylori TN2GF4 and were necropsied at 1, 3, 6, and 18 months. Main outcome measures: Bacterial clones recovered from the infected gerbils were evaluated by immunoblot for BabA expression, radioimmunoassay for Leb-binding, and bacterial binding to gastric tissue. H1 antigen expression and the increase in sialylation levels were monitored by immunohistochemistry. Results: BabA expression increased, then progressively decreased, and was completely absent by 6 months post-infection. Loss of BabA expression was caused by nucleotide changes/deletions within the babA gene that resulted in a truncated BabA. Infection with a BabA-expressing H. pylori caused severe mucosal injury, whereas infection with a BabA non-expressing strain caused only mild inflammation. In response to the infection, changes in the epithelial glycosylation pattern were observed, similar to responses observed in humans and monkeys. Conclusion: Down-regulation of BabA is probably a result of adaptation to the host response during long-term H. pylori infection. BabA expression is most likely not essential for colonisation, but for the obtained gerbil host response, which confirms the role of BabA adhesin as a virulence factor and its impact in the induction of a severe inflammatory response. The changes in glycosylation of gastric mucosa demonstrate the relevance of the Mongolian gerbil as a model for H. pylori infection and host responses.
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| 3. |
- Ohno, Tomoyuki, et al.
(författare)
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Effects of blood group antigen-binding adhesin expression during Helicobacter pylori infection of Mongolian gerbils
- 2011
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Ingår i: Journal of Infectious Diseases. - : Oxford University Press (OUP). - 0022-1899 .- 1537-6613. ; 203:5, s. 726-735
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Tidskriftsartikel (refereegranskat)abstract
- Helicobacter pylori outer membrane proteins, such as the blood group antigen-binding adhesin (BabA), are associated with severe pathological outcomes. However, the in vivo role of BabA during long-term infection is not clear. In this study, Mongolian gerbils were infected with H. pylori and necropsied continuously during 18 months. Bacterial clones were recovered and analyzed for BabA expression, Leb-binding activity, and adhesion to gastric mucosa. BabA expression was completely absent by 6 months post-infection. Loss of BabA expression was attributable to nucleotide changes within the babA gene that resulted in a truncated BabA. In response to the infection, changes in the epithelial glycosylation pattern were observed that were similar to responses observed in humans and monkeys. Furthermore, infections with BabA-expressing and BabA-nonexpressing H. pylori showed no differences in colonization, but infection with the BabA-expressing strain exhibited histological changes and increased inflammatory cell infiltration. This suggests that BabA expression contributes to severe mucosal injury.
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