Figure 3.
Figure 3. Functional defects in XID PMNs. (A) Phagocytosis of fluorescein-labeled, heat-killed bacteria by PMNs from WT (thin lines) or XID (thick lines) mice, shown as histograms of fluorescein intensity in gated Gr-1+ cells either not exposed to bacteria (-), or exposed to them at 4°C (4C) or at 37°C (37C) for one hour. (B) Time course of phagocytosis of fluorescein-labeled, heat-killed bacteria by peritoneal PMNs from WT or XID mice in gated Gr-1+ cells exposed to labeled bacteria at 37°C for varying times as indicated. (C) ROI responses of PMNs from WT (hollow symbols) or XID (filled symbols) mice to varying concentrations (μg/mL) of LPS over time as indicated (mean ± SE of triplicate cultures). (D) ROI responses of PMNs from WT or XID mice to PMA (30 ng/mL) over time (mean ± SE of triplicate cultures). (E) Induction of NO in PMNs from WT or XID mice to varying concentrations of LPS as indicated (mean ± SE of triplicate cultures). (F) Frequency of PMNs, either from blood or from peritoneal exudates induced by thioglycollate broth, expressing high levels of cell-surface CD80 or CD86 as indicated (mean ± SE). (G) Induction of PMN recruitment in the peritoneum of WT or XID mice in response to injection of oyster glycogen (OG) or thioglycollate broth (TG) 6 hours (OG) or 18 hours (TG) earlier, shown as PMNs rcovered per peritoneum (mean ± SE). (H) Time course of induction of PMN recruitment in the peritoneum of WT or XID mice in response to injection of thioglycollate broth at varying time points after injection, shown as PMNs recovered per peritoneum (mean ± SE). (I) Time course of motility of PMNs from WT or XID mice in vitro.

Functional defects in XID PMNs. (A) Phagocytosis of fluorescein-labeled, heat-killed bacteria by PMNs from WT (thin lines) or XID (thick lines) mice, shown as histograms of fluorescein intensity in gated Gr-1+ cells either not exposed to bacteria (-), or exposed to them at 4°C (4C) or at 37°C (37C) for one hour. (B) Time course of phagocytosis of fluorescein-labeled, heat-killed bacteria by peritoneal PMNs from WT or XID mice in gated Gr-1+ cells exposed to labeled bacteria at 37°C for varying times as indicated. (C) ROI responses of PMNs from WT (hollow symbols) or XID (filled symbols) mice to varying concentrations (μg/mL) of LPS over time as indicated (mean ± SE of triplicate cultures). (D) ROI responses of PMNs from WT or XID mice to PMA (30 ng/mL) over time (mean ± SE of triplicate cultures). (E) Induction of NO in PMNs from WT or XID mice to varying concentrations of LPS as indicated (mean ± SE of triplicate cultures). (F) Frequency of PMNs, either from blood or from peritoneal exudates induced by thioglycollate broth, expressing high levels of cell-surface CD80 or CD86 as indicated (mean ± SE). (G) Induction of PMN recruitment in the peritoneum of WT or XID mice in response to injection of oyster glycogen (OG) or thioglycollate broth (TG) 6 hours (OG) or 18 hours (TG) earlier, shown as PMNs rcovered per peritoneum (mean ± SE). (H) Time course of induction of PMN recruitment in the peritoneum of WT or XID mice in response to injection of thioglycollate broth at varying time points after injection, shown as PMNs recovered per peritoneum (mean ± SE). (I) Time course of motility of PMNs from WT or XID mice in vitro.

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