Epithelial mucins and bacterial adhesion - Carbohydrate Chemistry: Chemical and Biological Approaches - page 610

antigenicity and the immune system. But overall mucins present pre-
dominantly a protective barrier to keep bacteria away from epithelia. 86
Signals from bacterial side to the host regulate the expression of proteins
that decrease or increase biofilm formation. For example, Bacteroides
thetaiotaomicron stimulates the secretory lineage by mucus-secreting
goblet cells, whereas Faecalibacterium prausnitzii diminishes mucin gly-
cosylation. 87 Bacteria near mucosal surfaces take profit of increased
mucus secretion to form biofilms and live in this protected environment.
Initial bacterial adhesion prior to biofilm formation can be mediated for
example by the flagellar adhesin FliD from Pseudomonas aeruginosa. 88
The type b FliD as found in PAO1 strains, but not the type a as found in
PAK strains, has been shown specific for Le x and sLe x . 61 Fimbriae on
P. aeruginosa, named cup because of their biogenesis through the
chaperon-usher pathway, 89 have increased expression levels during the
subsequent biofilm formation in mucus layers. The fimbrial adhesin
CupB6 shows specificity for Le b on the CFG glycan array (http://
www.functionalglycomics.org/glycomics/ publicdata/selectedScreens.jsp).

5.1 Helicobacter and Campylobacter adhesins
Helicobacter pylori is a Gram-negative bacterium that infects over half of
the world's population. It was first isolated in 1983 by Marshall and
Warren from the gastric mucosa of patients with chronic gastritis. 90 Most
individuals acquire H. pylori in childhood. It induces a chronic inflam-
mation of the underlying mucosa, which tends to persist indefinitely
unless treated. If untreated, this organism participates in the develop-
ment of three important upper gastrointestinal diseases: gastroduodenal
ulcer, gastric carcinoma (except cancer of gastric cardia) and mucosal
associated lymphoid tissue (MALT) lymphoma. 91 The ability of the or-
ganism to cause disease depends on a variety of host, environmental and
bacterial factors.
H. pylori colonizes the gastric mucosa by adhering to epithelial cells
and the mucus layer lining the gastric epithelium. Although most
H. pylori reside within the mucous gel layer of the stomach that covers the
apical surface of the gastric epithelium, approximately 20% of the bac-
teria directly bind to gastric epithelial cells. 92 Different molecular
mechanisms have been proposed to explain bacterial adherence to the
gastric cells. Among them, two H. pylori adhesins have been well
characterized regarding their receptor interactions. BabA (blood group
antigen-binding adhesin) is specific for fucosylated blood group antigens
H-type 1 and Le b but also extends its spectrum of binding to terminal
residues of blood group A and B glycan determinants. 93-96 SabA (sialic-
acid binding adhesin) binds sLe a and sLe x antigens. 97-99 Although BabA
and SabA are the most prominent adhesins studied so far, it is important
to note that not all H. pylori strains express functional BabA or SabA
adhesins, 100,101 suggesting that other bacterial proteins may be involved
in adhesion to gastric cells.
Upon colonization, H. pylori induces a chronic, usually lifelong,

mucosal inflammation (gastritis) with concomitant expression of