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Burkholderia pseudomallei  is the causative agent of melioidosis and is a major mediator of sepsis in its endemic areas. Because of the low LD 50  via aerosols and resistance to multiple antibiotics, it is considered a Tier 1 select agent by the CDC and APHIS.  B. pseudomallei  is an encapsulated bacterium that can infect, multiply, and persist within a variety of host cell types.  In vivo  studies suggest that macrophages and neutrophils are important for controlling  B. pseudomallei  infections, however few details are known regarding how neutrophils respond to these bacteria. Our goal is to describe the capacity of human neutrophils to control highly virulent  B. pseudomallei  compared to the relatively avirulent, acapsular  B. thailandensis  using  in vitro  analyses.  B. thailandensis  was more readily phagocytosed than  B. pseudomallei , but both displayed similar rates of persistence within neutrophils, indicating they possess similar inherent abilities to escape neutrophil clearance. Serum opsonization studies showed that both were resistant to direct killing by complement, although  B. thailandensis  acquired significantly more C3 on its surface than  B. pseudomallei , whose polysaccharide capsule significantly decreased the levels of complement deposition on the bacterial surface. Both  Burkholderia  species showed significantly enhanced uptake and killing by neutrophils after critical levels of C3 were deposited. Serum-opsonized  Burkholderia  induced a significant respiratory burst by neutrophils compared to unopsonized bacteria, and neutrophil killing was prevented by inhibiting NADPH-oxidase. In summary, neutrophils can efficiently kill  B. pseudomallei  and  B. thailandensis  that possess a critical threshold of complement deposition, and the relative differences in their ability to resist surface opsonization may contribute to the distinct virulence phenotypes observed  in vivo .

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Capsule Influences the Deposition of Critical Complement C3 Levels Required for the Killing of Burkholderia pseudomallei via NADPH-Oxidase Induction by Human Neutrophils