Abstract
Monoclonal antibodies against E. coli type 1 pili and the K13 capsular polysaccharide strongly influenced the interaction between human polymorphonuclear leukocytes (PMNL) and E. coli 06:K13:H1. Bacteria with type 1 pili, associated with the neutrophils caused a metabolic activation but were not ingested. Addition of monoclonal antibodies to type 1 pili resulted in increased association, but also phagocytosis and metabolic activation of the granulocytes. Monoclonal antibodies against the K13 polysaccharide strongly stimulated phagocytosis, especially of the type 1 piliated bacteria, suggesting a synergistic effect between binding of type 1 pili and the Fc part of the capsular antibodies to the PMNL. Addition of D-mannose inhibited the opsonization of type 1 piliated E. coli 06:K13:H1 in the presence of both type 1 pilus antibodies and capsular antibodies. Monoclonal anti-idiotypic (anti-anti-capsular) antibodies reduced the association with the PMNL of the bacteria preopsonized with anti-capsular antibodies. The bacterial ingestion and the metabolic activation of the PMNL were also reduced, suggesting a role for anti-idiotypic antibodies in specific modulation of inflammation.