pagPIs Required for Resistance to Antibody-Mediated Complement Lysis duringBordetella bronchisepticaRespiratory Infection

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Abstract
To efficiently colonize and persist in the lower respiratory tract, bacteria must survive multiple host immune mechanisms.Bordetella bronchisepticais a gram-negative respiratory pathogen that naturally infects mice and persists in the lower respiratory tract for up to 49 days postinoculation. In this work, we examined the effect of mutation of thepagPgene on the persistence ofB. bronchisepticain the lower respiratory tract of mice. ThepagPgene encodes a palmitoyl transferase that is responsible for the addition of a palmitoyl group to the lipid A region ofB. bronchisepticalipopolysaccharide. Data presented here confirm that aB. bronchisepticaΔpagPmutant demonstrates defective persistence in the lower respiratory tract of wild-type mice. We hypothesized that the defective persistence of theB. bronchisepticaΔpagPmutant was due to an increased susceptibility of this mutant to a host immune response. In vivo data indicate that both B cells and the complement component C3 are required for the reduced bacterial numbers of the ΔpagPmutant on day 14 postinoculation. In addition, an in vitro complement killing assay demonstrated thatB. bronchisepticaexhibitspagP-dependent resistance to antibody-mediated complement killing at low concentrations of immune serum. Taken together, these results suggest thatpagPis required forB. bronchisepticato resist antibody-mediated complement lysis during respiratory infection.