An enzymatic ruler modulates Lewis antigen glycosylation of Helicobacter pylori LPS during persistent infection

PNAS 103:2863-68, 2006

Speaker:洪惠雯                          Date: 2006 /9/27

Commentator:何漣漪  教授              Time:13:10~14:00  Room:601

Abstract:

    The human Gram-negative bacterium Helicobacter pylori (H.pylori) is able to persist for a lifetime on the gastric mucosa of 50% of the world population. In most individuals, colonization results in uncomplicated chronic gastritis, but in some patients H. pylori infection leads to peptic ulcer disease and gastric cancer. The LPS (lipopolysaccaride) of most H. pylori strains contains fucosylated oligosaccharides that mimic Lewis antigens present in humans and the expression of these antigens can be phase variable which are regulated via slipped-strand mispairing in intragenic polyC tract regions in the population of a single strain. In addition, the three fucosyltransferases (FucT) , FutC, does not possess a variable C-terminal region. However, FutA and FutB contain a C-terminal tandem repeat region, consisting of a variable number of a 7-aa sequence, DD/NLRV/INY. Finally, the authors demonstrated that the variation of LPS is decorated by C-terminal tandem hepatad-repeat region in FutA and FutB. The number of C-terminal tandem hepatad-repeat region is able to constitute a mechanism to decide the LPS O-antigen units.

Reference:

1.Nilsson C, Skoglund A, Moran AP, Annuk H, Engstrand L, Normark S.(2006)  An enzymatic ruler modulates Lewis antigen glycosylation of  Helicobacter pylori LPS during persistent infection. Proc Natl Acad Sci U S A. 2006 103:2863

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