The proportion and number of peripheral blood CD3⁻ CD56⁺ NK cells in SIRS and
sepsis groups were normal, and no statistical difference was found when compared with those of the healthy control group [cell proportion: 0.102 ± 0.019, 0.102 ± 0.108 vs. 0.106 ± 0.018, F = 0.018, P = 0.982; cell number (× 10⁶/L): 182.46 ± 65.98, 172.97 ± 63.51 vs. 179.25 ± 60.44, F=0.349, P=0.706]. It was shown by NK cell degranulation detection that there was no significant difference in the expression of CD107 and
interferon-γ (IFN-γ) secretion [CD107: 0.135 ± 0.050, 0.140 ± 0.058, 0.128 ± 0.070, F = 0.583, P = 0.560; IFN-γ (kU/L): 14.36 ± 4.74, 12.49 ± 4.21, 13.45 ± 5.04, F=1.616, P=0.202] among healthy control group, SIRS group, and
sepsis group. It was shown by antibody dependent cytotoxic effect (ADCC) test that there was no difference in the expression of CD107 among healthy control group, SIRS group, and
sepsis group (0.574 ± 0.166, 0.643 ± 0.165, 0.581 ± 0.157, F = 0.808, P = 0.448). When compared with healthy controls, the secretion of IFN-γ was increased in SIRS patients (kU/L: 40.5 ± 13.2 vs. 28.4 ± 9.6, P = 0.001), while reduced in
sepsis patients (kU/L: 19.8 ± 6.7 vs. 28.4 ± 9.6, P<0.01). Compared with SIRS group, only NK cell surface inhibitory receptors CD158e (KIR 3DL1) expression in
sepsis group was significantly increased (0.203 ± 0.057 vs. 0.079 ± 0.021, t = 15.762, P<0.001), and there were no significant differences in the other phenotype between the two groups. Compared with SIRS group, the IFN-γ production of the
sepsis group was significantly lowered (kU/L: 0.280 ± 0.040 vs. 0.310 ± 0.038, t = 3.390, P = 0.009), and the level of
IL-12 was also significantly decreased (ng/L: 0.15 ± 0.03 vs. 0.30 ± 0.08, t = 32.832, P < 0.001).
CONCLUSIONS: