Molecular Basis of Bacterial Infections (BMW33416)
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Molecular Basis of Bacterial Infections Evelien Floor
Host defense at the mucosal
surface
Many bacteria in the intestinal tract are commensal. However, there are also enteropathogenic
bacteria present, those are the bacteria that cause infection. Bacteria in the intestinal lumen have to
encounter different layers to cause systemic infection:
Mucus layer
o Gel-forming mucins
o Anti-microbial peptides
o IgA antibodies
Epithelial monolayer (enterocytes)
o Transmembrane mucin
o Toll like receptors
o Cytokine secretion
Innate immune cells
o Dendritic cells
o Macrophages
o Neutrophils
In the mucus layer there is a gradient antimicrobial peptides and IgA which creates two mucus layers:
the outer mucus with commensal bacteria followed by the inner mucus without bacteria. Many
bacteria in the intestine consist of flagella because they are important to swim through the mucus
layer.
Gel-forming mucins
The thickness of the mucus layer is different
throughout the intestinal tract. The mucus thickness
tells something about the nutrient uptake and the
number of bacteria present. The thicker the mucus
layer the less nutrient uptake and the more bacteria
present (physical barrier). The mucus layer in the
colon for instance is very thick.
The composition of mucus:
1% mucins and Trefoil factor peptides
1% free protein (IgA)
1% dialyzable salts
>95% water
Mucins in mucus are O-linked glycosylated.
The most important terminal sugars are
sialic acid and fucose. Commensal bacteria
feed on mucin sugars and do not invade. The
mucus layer therefore forms a physical
barrier and provides nutrients. When an
individual gets sick the mucin glycosylation is
altered: there are more fucoses to feed the
bacteria.
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