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Effects of BabA exp...
Effects of BabA expression during H. pylori infection of Mongolian gerbils
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- Ohno, Tomoyuki (författare)
- Department of Medicine-Gastroenterology, Michael E. DeBakey Vetrans Medical Center and Baylor College of Medicine, Houston, Texas, USA
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- Vallström, Anna, 1979- (författare)
- Umeå universitet,Institutionen för medicinsk kemi och biofysik,Oral mikrobiologi
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Wu, MJ (författare)
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- Rugge, Massimo (författare)
- Department of Diagnostic Science and Special Therapies (Pathology Unit), University of Padova, Padova, Italy
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- Ota, Hiroyoshi (författare)
- Department of Biomedical Laboratory Sciences, School of Health Sciences, Shinshu University School of Medicine, Matsumoto, Japan
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- Graham, David Y (författare)
- Department of Medicine-Gastroenterology, Michael E. DeBakey Vetrans Medical Center and Baylor College of Medicine, Houston, Texas, USA
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- Arnqvist, Anna (författare)
- Umeå universitet,Institutionen för medicinsk kemi och biofysik
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- Yamaoka, Yoshio (författare)
- Department of Medicine-Gastroenterology, Michael E. DeBakey Vetrans Medical Center and Baylor College of Medicine, Houston, Texas, USA and Department of Environmental and Preventive Medicine, Oita University Faculty of Medicine, Yufu, Japan
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Department of Medicine-Gastroenterology, Michael E DeBakey Vetrans Medical Center and Baylor College of Medicine, Houston, Texas, USA Institutionen för medicinsk kemi och biofysik (creator_code:org_t)
- Engelska.
- Relaterad länk:
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https://urn.kb.se/re...
Abstract
Ämnesord
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- 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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