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Helicobacter pylori evolution and phenotypic diversification in a changing host

Helicobacter pylori evolution and phenotypic diversification in a changing host. Sebastian Suerbaum & Christine Josenhans. Asolina Braun 11.01.2010. Barry Marshall & Robin Warren, 1982 colonizes the stomach link to gastritis and ulcers Marshall ingests H. pylori => gastritis

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Helicobacter pylori evolution and phenotypic diversification in a changing host

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  1. Helicobacter pylori evolution and phenotypic diversification in a changing host Sebastian Suerbaum & Christine Josenhans Asolina Braun 11.01.2010

  2. Barry Marshall & Robin Warren, 1982 colonizes the stomach link to gastritis and ulcers Marshall ingests H. pylori => gastritis 2005 Nobel prize „for their discovery of the bacterium H. pylori and its role in gastritis and peptic ulcer disease” History

  3. colonizes 50% of the world‘s population infection during infancy via family members Clinics 5,5% of all cancer cases

  4. extreme genetic diversity mutagenesis recombination host interaction outstanding evation of immune system immune suppression Success Strategy

  5. extraordinary genetic heterogeneity every infected individual harbors their own strain(s) strains change during infection high recombination events (multilocus enzyme electrophoresis data, homoplasy test) Diversity

  6. Geographical Distribution • data based on multilocus sequence typing

  7. defect mismatch repair defect base excision repair long repetitive sequences => frameshift altered expression if located inside regulators intragenomic deletions/rearrangements Diversification by Mutagenesis

  8. recombination of short DNA fragments (~417 bp vs. 2-10 kbp) 50% exchange of genome in 40 years 1,111 conserved genes + ~400 frequent gene exchange seldom gene loss/gain (1 in 650 events) Diversification by Recombination

  9. BabA and SabA adhesins bind Lewis b and sialyl-Lewis on epithelium phase-variable expression adaptation to niches, acid conditions, … geographical correlation with blood groups Host Interaction

  10. vacuolating cytotoxin (Vac A) vacuolation, tissue damage inhibits proliferation of T cells inhibits antigen presentation by B cells LPS Lewis antigens (on O-antigen side chains) binding of H. pylori to DCs via DC-SIGN => TH1 response diminished, ↓IL6, ↑IL10 => immune suppression heterogenous expression Host Interaction

  11. flagellar motility implications unknown cag PAI (a chromosome segment) type IV SS destruction of the basal membrane atrophic gastritis, peptic ulcers, adenocarcinoma (Ishikawa et al., PNAS, 2005) Host Interaction

  12. prevalence in Western countries declines due to less mixed infections? due to better hygiene, antibiotics, broccoli? vaccination (Cag A) Outlook

  13. high prevalence of 50% extreme genetic diversity defective mutation repair systems many repetitive regions prone to mutations many recombination events outstanding evation of immune system BabA and SabA Vac A LPS Cag PAI Summary

  14. Thank you for your attention

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