Bordetella parapertussis survives the innate interaction with human neutrophils by impairing bactericidal trafficking inside the cell through a lipid raft-dependent mechanism mediated by the lipopolysaccharide O antigen.

GORGOJO, JUAN PABLO; LAMBERTI, YANINA; VALDEZ, HUGO; HARVILL, ERIC; RODRIGUEZ, MARÍA EUGENIA

INFECTION AND IMMUNITY

AMER SOC MICROBIOLOGY

Lugar: Washington; Año: 2012 vol. 80 p. 4309 - 4316

0019-9567

Whooping cough is a reemerging disease caused by two closely related pathogens, Bordetella pertussis and Bordetella parapertussis. The incidence of B. parapertussis in whooping cough cases has been increasing since the introduction of acellular pertussis vaccines containing purified antigens common to both strains. Recently published results demonstrated that these vaccines do not protect against B. parapertussis due to the presence of the O antigen on the bacterial surface that impairs antibody access to shared antigens. We here investigated the effect of the lack of opsonization of B. parapertussis on the outcome of its interaction with human neutrophils (PMN). In the absence of opsonic antibodies PMN interaction with B. parapertussis resulted in a non-bactericidal trafficking upon phagocytosis. A high percentage of non-opsonized B. parapertussis was found in non-acidic lysosome marker (LAMP)-negative phagosomes with access to the host cell recycling pathway of external nutrients, allowing bacterial survival as determined by intracellular CFU counts. The LPS O antigen was found involved in directing B. parapertussis to PMN lipid rafts eventually determining this non-bactericidal fate inside the PMN. IgG-opsonization of B. parapertussis drastically changed this interaction not only by inducing efficient PMN phagocytosis but also by promoting PMN bacterial killing. These data provide new insights into the host immune mechanisms against B. parapertussis, and document the crucial importance of opsonic antibodies in immunity to this pathogen.