1. Helicobacter pylori SabA Adhesin in Persistent Infection and Chronic Inflammation
Science 297, , 2002

2. Helicobacter pylori is a Gram-negative bacterium that colonizes the human stomach, mainly persisting within the gastric mucus layer.
Chronic infection is associated with the development of gastric adenocarcinoma, and H. pylori was recently defined as a class I carcinogen.

3. Adhesins are microorganisms’ surface protein that interact with glycoproteins, proteoglycans, and glycolipids. The functions of microoragnisms’ adhesins are cell attachment, tissue colonization, and invasion. The best defined H. pylori adhesin found to date is Leb blood group antigen binding adhesin (BabA). BabA bind to fucosylated blood group antigens Lewis B (Leb) and H-1.

6. Representive of Lewis structure

8. babA1A2 (+)
BabA1A2 (-)
Infected cells
Leb mAb
stain
Inhibition with Leb
sLex mAb
stain
Inhibition with sLex
Noninfected cells
sLex mAb stain
babA1A2 (+)
BabA1A2 (-)
Fig. 1
The sLex antigen confers adherence of H. pylori-infected (strain Wu 12) human gastric mucosa.

9. Fig. 2A H/E stain of transgenic Leb mouse gastric mucosa babA1A2 (+)
sLex mAb stain
Inhibition with sLex
Fig. 2A

10. Fig. 2B 1. Calf brain 2. Human neutrophile granulocytes
Chemically stained
Probed with sLex mAb
1. Calf brain
2. Human neutrophile granulocytes
3. Desialylation of #2
4. Adenocarcinoma
5. Desialytion of #4
6. sdiLex GSL
7. sLea GSL
8. S(mono) Lex GSL
9. Leb GSL
Probed with babA1A2(+)
Probed with babA1A2(-)
Fig. 2B

12. Fig. 2C

13. Fig. 3 H. pylori binds to sialyted antigens

14. Fig. 3 H. pylori binds to sialyted antigens
Leb mouse gastric mucosa
Human gastric mucosa
Fig. 3 H. pylori binds to sialyted antigens

15. Fig. 4 Infection induces expression of sLex antigens

16. Fig. 5 Retagging of SabA

18. J99 sabA mutant
Control
Preatment with Leb
Fig. 5B

19. Fig. 5C J99 wild type J99 sabA mutant J99 babA mutant J99 babA/sabA

20. Fig. 6