Host-parasite interactions between Bordetella pertussis and human polymorphonuclear leukocytes.

Little is known regarding the interaction of Bordetella pertussis with polymorphonuclear leukocytes (PMNL) or the role PMNL play as an initial line of defense against B. pertussis infection. An in vitro system was developed to establish optimum conditions for the study of phagocytosis and killing of three virulent strains of B. pertussis and a series of derivative mutants using strictly human PMNL and sera. Optimum phagocytosis of B. pertussis occurred by opsonization with human anti-B. pertussis antibody (HAPA), while autologous normal sera (NS) did not induce significant phagocytosis. An antiserum made in rabbits against an avirulent strain was required as an opsonin for significant phagocytosis of several avirulent strains. Over 50% of all B. pertussis strains and mutants tested survived PMNL bactericidal activities while Escherichia coli controls were readily killed. Therefore, if internalized, B. pertussis has an innate ability to survive within human PMNL. No one virulence factor appears to be superior to another in determining survivability. Electron microscopic studies using acid phosphatase as a lysosomal marker demonstrated that virulent B. pertussis strains are capable of surviving intracellularly within PMNL phagosomes and that such survival is due to inhibition of phagosome-lysosome fusion. PMNL respiratory burst activity is unaffected by internalized B. pertussis. This strongly suggests that inhibition of phagosome-lysosome fusion is the key mechanism of B. pertussis intracellular survival within PMNL