Fig. 1.

Interaction of bacterial pathogens with human PMNs. (A) Phagocytosis of L. monocytogenes, Bkl. cepacia, Sta. aureus, and Str. pyogenes by human neutrophils. *, P < 0.001 vs. all bacteria; **, P ≤ 0.04 vs. all bacteria except heat-killed (Δ) Str. pyogenes. Results are the mean ± SD of three to five experiments. (B) Phagocytosis of Bor. hermsii.(Top) Number of PMNs with bound (black square) and/or ingested (green circle) Bor. hermsii. AI, association index; PI, phagocytic index. Micrographs (Right) illustrate ingestion and degradation of Bor. hermsii over time despite the appearance of extracellular staining (Extracellular, red). All Bor. hermsii, ingested, bound and extracellular (green). (Magnifications: ×400, Left; ≈×800, Right.) (C) PMN ROS production. The rate of ROS production for each pathogen is the mean of three separate experiments. ΔFL, change in fluorescence. (D) Killing of pathogens by human PMNs. At each time, PMNs were lysed and bacteria were plated on growth agar. Colonies were enumerated the next day, and percent bacteria killed was calculated as described in Supporting Methods. Results are the mean ± SD of three separate experiments. Bor. hermsii does not reliably form colony-forming units, and, thus, it was not possible to accurately assess PMN killing.