Figure 2.
Killing of PsA by normal PMNs is chloride dependent. Normal human peripheral blood PMNs were allowed to ingest serum-opsonized PsA (20:1 PsA:PMN) in sodium gluconate chloride-free Ringer’s buffer containing 10% dialyzed human AB serum for 20 minutes at 37°C. The uningested PsAs were removed by low-speed centrifugation, and the cell pellets containing PMNs harboring PsA resuspended in Ringer’s buffer containing varied concentrations of chloride (0-127 mM) and 10% dialyzed serum. After the zero time point was sampled to determine the initial number of viable PsAs, PsA-laden PMNs were incubated with shaking at 37°C, and aliquots were taken at the indicated time points (10, 20, 30, and 40 minutes). The fraction of viable PsAs relative to those at zero time point was determined. The data are plotted on a semi-log scale relative to the viable bacteria present at zero time. [Cl], chloride concentration; K, killing rate constant.

Killing of PsA by normal PMNs is chloride dependent. Normal human peripheral blood PMNs were allowed to ingest serum-opsonized PsA (20:1 PsA:PMN) in sodium gluconate chloride-free Ringer’s buffer containing 10% dialyzed human AB serum for 20 minutes at 37°C. The uningested PsAs were removed by low-speed centrifugation, and the cell pellets containing PMNs harboring PsA resuspended in Ringer’s buffer containing varied concentrations of chloride (0-127 mM) and 10% dialyzed serum. After the zero time point was sampled to determine the initial number of viable PsAs, PsA-laden PMNs were incubated with shaking at 37°C, and aliquots were taken at the indicated time points (10, 20, 30, and 40 minutes). The fraction of viable PsAs relative to those at zero time point was determined. The data are plotted on a semi-log scale relative to the viable bacteria present at zero time. [Cl], chloride concentration; K, killing rate constant.

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