Fig. 6.
Fig. 6. Effect of rhIL-10 on neutrophil apoptosis modulated through LPS and/or proinflammatory cytokines. Freshly isolated neutrophils (1 × 106/mL) from healthy humans were cultured with rhTNF-α (1,000 U/mL), rhIFN-γ (10 ng/mL), rhG-CSF (10 ng/mL), or rhGM-CSF (10 ng/mL) in the presence or absence of rhIL-10 (100 U/mL) and LPS (1 μg/mL) for 16 hours. Neutrophil apoptosis was analyzed by flow cytometry after permeabilization with ethanol and staining with PI. Data are reported as the percentage of fragmented nuclei reflecting the relative proportion of apoptotic cells. Results in each figure represent the mean ± SEM of three separate experiments performed with neutrophils isolated from three different healthy individuals. *P < .05 without agent versus LPS/rhTFN-α/rhIFN-γ/rhG-CSF/rhGM-CSF; ‡P < .05 without rhIL-10 versus with rhIL-10.

Effect of rhIL-10 on neutrophil apoptosis modulated through LPS and/or proinflammatory cytokines. Freshly isolated neutrophils (1 × 106/mL) from healthy humans were cultured with rhTNF-α (1,000 U/mL), rhIFN-γ (10 ng/mL), rhG-CSF (10 ng/mL), or rhGM-CSF (10 ng/mL) in the presence or absence of rhIL-10 (100 U/mL) and LPS (1 μg/mL) for 16 hours. Neutrophil apoptosis was analyzed by flow cytometry after permeabilization with ethanol and staining with PI. Data are reported as the percentage of fragmented nuclei reflecting the relative proportion of apoptotic cells. Results in each figure represent the mean ± SEM of three separate experiments performed with neutrophils isolated from three different healthy individuals. *P < .05 without agent versus LPS/rhTFN-α/rhIFN-γ/rhG-CSF/rhGM-CSF; P < .05 without rhIL-10 versus with rhIL-10.

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