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Chapter 35 : Lipopolysaccharide Lewis Antigens

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Abstract:

As determined by serological techniques, the O-antigen of lipopolysaccharide (LPS) of more than 80% of strains tested worldwide express Lewis blood group antigens. Several host lectins are known to interact with host Lewis antigens; the same lectins may interact with Lewis antigens. This chapter discusses phase variation of LPS, including LPS biosynthesis and genetics; the biological significance of Lewis antigen mimicry; and the role of Lewis antigens in interactions of with host lectins. Antigastric autoantibodies present in sera of -infected patients are directed to gastric parietal canaliculi, but absorption with does not diminish autoantibody reactivity. Selection and outgrowth of Le LPS variants would be driven by anti-Le antibodies, and these are not found in infected patients. Studies on the biological role of Lewis antigens have largely taken place through insertional mutagenesis of LPS biosynthesis genes. In summary, the mechanisms of LPS phase variation are known in detail; knowledge of the biological role of Lewis antigens and phase variation therein is in its infancy, but a role in adhesion seems likely.

Citation: Appelmelk B, Vandenbroucke-Grauls C. 2001. Lipopolysaccharide Lewis Antigens, p 419-428. In Mobley H, Mendz G, Hazell S (ed), . ASM Press, Washington, DC. doi: 10.1128/9781555818005.ch35

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Figure 1

LPS phase variation in LPS. strain B1.5 was colony-blotted with an anti-H type 1 MAb and immuno-stained.

Citation: Appelmelk B, Vandenbroucke-Grauls C. 2001. Lipopolysaccharide Lewis Antigens, p 419-428. In Mobley H, Mendz G, Hazell S (ed), . ASM Press, Washington, DC. doi: 10.1128/9781555818005.ch35
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Image of Figure 2
Figure 2

Characterization of LPS phase variants by SDS-PAGE visualized by silver stain (a); immunoblot with anti-Le MAb (b); and anti-Le MAb (c). Lane 1, NCTC 11637; lane 2, variant 1b; lane 3, variant lc; lane 4, variant 2b; lane 5, variant 3a. The low molecular weight fraction in (a) represents the core-lipid A moiety.

Citation: Appelmelk B, Vandenbroucke-Grauls C. 2001. Lipopolysaccharide Lewis Antigens, p 419-428. In Mobley H, Mendz G, Hazell S (ed), . ASM Press, Washington, DC. doi: 10.1128/9781555818005.ch35
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Figure 3

Molecular mimicry between LPS and gastric H,K-ATPase. Mouse or human gastric H,K-ATPase (in concentrations of 2 to 10 µg per lane) were subjected to SDS-PAGE and immunoblotted with monoclonal antibodies specific for Le(below), Le (middle), and peptide epitopes of the (3-chain (upper panel), respectively. Due to heterogeneity in glycosylation, the fS-chain appears as a smear.

Citation: Appelmelk B, Vandenbroucke-Grauls C. 2001. Lipopolysaccharide Lewis Antigens, p 419-428. In Mobley H, Mendz G, Hazell S (ed), . ASM Press, Washington, DC. doi: 10.1128/9781555818005.ch35
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Tables

Generic image for table
Table 1

Structures of Lewis blood group antigens and glycosyltransferases required for biosynthesis

Citation: Appelmelk B, Vandenbroucke-Grauls C. 2001. Lipopolysaccharide Lewis Antigens, p 419-428. In Mobley H, Mendz G, Hazell S (ed), . ASM Press, Washington, DC. doi: 10.1128/9781555818005.ch35
Generic image for table
Table 2

LPS phase variants of strains NCTC 11637 and P466

Citation: Appelmelk B, Vandenbroucke-Grauls C. 2001. Lipopolysaccharide Lewis Antigens, p 419-428. In Mobley H, Mendz G, Hazell S (ed), . ASM Press, Washington, DC. doi: 10.1128/9781555818005.ch35
Generic image for table
Table 3

Reactivity of monoclonal antibodies with strains in relation to α3-fucosyltransferase gene C-tract length

Citation: Appelmelk B, Vandenbroucke-Grauls C. 2001. Lipopolysaccharide Lewis Antigens, p 419-428. In Mobley H, Mendz G, Hazell S (ed), . ASM Press, Washington, DC. doi: 10.1128/9781555818005.ch35

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