Figure 3.
Lack of chloride influx in phagosomes of CF PMNs. Serum-opsonized zymosan particles covalently conjugated with a chloride probe (MQHA, 6-methoxyquinoline-N-6-hexanoic acid) and reference probe (TMR, tetramethylrhodamine) were ingested by normal or CF PMNs. Intraphagosomal chloride levels were continuously measured by quantitative fluorescence microscopy. The probe-laden cells were bathed in different chloride buffers in the following order: (1) sodium gluconate chloride-free Ringer’s buffer (NaGlu R), (2) sodium chloride (135 mM) Ringer’s buffer (NaCl R), and (3) chloride-free Ringer’s buffer (NaGlu R). The phagosomal chloride concentration of normal PMNs (○) rapidly respond to the change in extracellular chloride change, whereas that of CF PMN (●) had no response. At 30 minutes, a series of isoosmotic 0.1% Triton X-100 solutions containing varied chloride concentrations (0-135 mM) was introduced sequentially to calibrate the system at 6-minute intervals. Reprinted from reference 86.

Lack of chloride influx in phagosomes of CF PMNs. Serum-opsonized zymosan particles covalently conjugated with a chloride probe (MQHA, 6-methoxyquinoline-N-6-hexanoic acid) and reference probe (TMR, tetramethylrhodamine) were ingested by normal or CF PMNs. Intraphagosomal chloride levels were continuously measured by quantitative fluorescence microscopy. The probe-laden cells were bathed in different chloride buffers in the following order: (1) sodium gluconate chloride-free Ringer’s buffer (NaGlu R), (2) sodium chloride (135 mM) Ringer’s buffer (NaCl R), and (3) chloride-free Ringer’s buffer (NaGlu R). The phagosomal chloride concentration of normal PMNs (○) rapidly respond to the change in extracellular chloride change, whereas that of CF PMN (●) had no response. At 30 minutes, a series of isoosmotic 0.1% Triton X-100 solutions containing varied chloride concentrations (0-135 mM) was introduced sequentially to calibrate the system at 6-minute intervals. Reprinted from reference 86.

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