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. 2014 Aug;184(8):2297–2309. doi: 10.1016/j.ajpath.2014.05.002

Figure 2.

Figure 2

Role of β-arrestin-1 (βArr1) in cellular infiltration and bacterial killing. Wild-type (WT; white bars), βArr1 knockout (KO; β-Arr1−/−; black bars), and βArr1 heterozygous (β-Arr1+/−; gray bars) mice underwent sham or cecal ligation and puncture surgeries and were euthanized at the defined time points. A: Neutrophil and macrophage infiltration in the peritoneal cavity of sham mice at 24 hours and septic mice at indicated time points after surgery were determined using flow cytometry. B: Bacterial load was represented as colony-forming units (CFU)/mL in the blood of septic mice at the indicated time points and grades of sepsis. C: Bacterial killing capacity of thioglycollate-elicited neutrophils from WT and KO mice was depicted as surviving bacteria (CFU) recovered from the extracellular medium at the indicated time points for total bacterial killing, and from cellular lysate at various time points after 20 minutes uptake for the intracellular killing assay. Data for septic mice were pooled from three independent experiments. n = 9 to 14 for septic mice and n = 3 for sham (B); n = 3 to 5 (C). Error bars denote SEM. ∗P < 0.05 using Student's t-test. 16G-SP, 16-guage needle single puncture; 20G-DP, 20-guage needle double puncture.