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. 2018 Aug 20;128(9):4115–4131. doi: 10.1172/JCI64772

Figure 7. Increased phagocytosis rate, normal killing of bacteria, and dysregulated ROS responses in XLN neutrophils.

Figure 7

E. coli (A) and S.aureus (B) killing capacity of WT and WASp XLN neutrophils were assessed by coincubating serum-opsonized bacteria and neutrophils at a ratio of 1:5 (E. coli/neutrophil) for 60 minutes (A) or 1:1 (S.aureus/neutrophil) for 60 and 90 minutes as shown in upper and lower panels, respectively (B). n = 3 replicates, n = 3 experiments with each bacteria. (C and D) Phagocytosis of Alexa Fluor 488–labeled, serum-opsonized E. coli (C) and S. aureus (D) by WT WASp XLN neutrophils measured by flow cytometry. n = 3 replicates, n = 3 experiments with each bacteria. (E–G) Intracellular ROS (IC ROS) measured with luminol chemiluminescence in murine bone marrow neutrophils upon stimulation with E. coli (n = 8) (E), S.aureus (n = 10) (F), or PMA (n = 18). n = 4. Data are shown as mean ± SD, 2-way ANOVA. (H–J) Extracellular ROS (EC ROS) was measured using a lucigenin chemiluminescence assay in murine bone marrow neutrophils upon stimulation with (H) heat-killed serum-opsonized S. aureus (n = 18), (I) fMLP (n = 4), or (J) PMA (n = 26). n = 4. Data are shown as mean ± SD. Two-way ANOVA. (K) Extracellular ROS was measured upon PMA stimulation of murine (upper panel) and human healthy donor (lower panel) neutrophils with or without pretreatment with jasplakinolide. n = 5. Data are shown as mean ± SD. *P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001.