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Adherence is often an essential step in bacterial pathogenesis, required for colonizing a new host. To effectively adhere to host surfaces, many bacteria produce multiple adherence factors called adhesins. For example, nontypeable Haemophilus influenzae expresses the adhesins Hia, Hap, Oap and a hemagglutinating pili.

Adhesins are attractive vaccine candidates because they are often essential to infection and are surface-located making them readily accessible to antibodies.

Escherichia coli

The effectiveness of anti-adhesin antibodies is illustrated by studies with FimH, the adhesin of uropathogenic Escherichia coli (UPEC). In animal models, passive immunization with anti FimH-antibodies and vaccination with the protein significantly reduced colonization by UPEC. Moreover, the Bordetella pertussis adhesins FHA and Pertactin are components of 3 of the 4 acellular pertussis vaccines currently licensed for use in the U.S. Thus, adhesins are proven, effective vaccines. [1]

H. pylori ABO Blood Group Antigen Binding Adhesin

Adherence by Helicobacter pylori increases the risk of gastric disease. Here, we report that more than 95% of strains that bind fucosylated blood group antigen bind A, B, and O antigens (generalists), whereas 60% of adherent South American Amerindian strains bind blood group O antigens best (specialists). This specialization coincides with the unique predominance of blood group O in these Amerindians. Strains differed about 1500-fold in binding affinities, and diversifying selection was evident in babA sequences. We propose that cycles of selection for increased and decreased bacterial adherence contribute to babA diversity and that these cycles have led to gradual replacement of generalist binding by specialist binding in blood group O–dominant human populations.[2]

Helicobacter pylori adhesin binding fucosylated histo-blood group antigens revealed by retagging

Ilver D, Arnqvist A, Ogren J, Frick IM, Kersulyte D, Incecik ET, Berg DE, Covacci A, Engstrand L, Boren T Science 1998 Jan 16;279(5349):373-377 Department of Microbiology, Umea University, SE-901 87 Umea, Sweden. The bacterium Helicobacter pylori is the causative agent for peptic ulcer disease. Bacterial adherence to the human gastric epithelial lining is mediated by the fucosylated Lewis b (Leb) histo-blood group antigen.