Hemagglutination byB. fragilisis mediated by capsular polysaccharides and is influenced by host ABO blood type

Abstract

Bacterial hemagglutination of red blood cells (RBCs) is mediated by interactions between bacterial cell components and RBC envelope glycans that vary across individuals by ABO blood type. ABO glycans are also expressed on intestinal epithelial cells and in most individuals secreted into the intestinal mucosa, indicating that hemagglutination by bacteria may be informative about bacteria-host interactions in the intestine. Bacteroides fragilis, a prominent member of the human gut microbiota, can hemagglutinate RBCs by an unknown mechanism. Using a novel technology for quantifying bacterial hemagglutination, genetic knockout strains of B. fragilis and blocking antiserums, we demonstrate that the capsular polysaccharides of B. fragilis, polysaccharide B (PSB), and PSC are both strong hemagglutinins. Furthermore, the capacity of B. fragilis to hemagglutinate was much stronger in individuals with Type O blood compared to Types A and B, an adaptation that could impact the capacity of B. fragilis to colonize and thrive in the host.

Acceptive Immunity: The Role of Fucosylated Glycans in Human Host–Microbiome Interactions

“…The highest hemagglutination has been observed for blood group antigen O, and less for the A and B groups. PSC expression is believed to be an independent PSB duplicating system for colonization and hemagglutination [ 146 ]. PSA is non-covalently bound with PSB in the capsule [ 144 ].…”