Polymicrobial sepsis influences NK-cell-mediated immunity by diminishing NK-cell-intrinsic receptor-mediated effector responses to viral ligands or infections
Fig 4
Sepsis impairs NK-cell capacity to produce IFN-γ in response to L. monocytogenes infection and cytokine stimulation.
(A) Experimental Design. 2 days after sham or CLP surgery mice were infected with of virulent Listeria monocytogenes (L.m. - 104 CFU, i.v.). The frequency or number of NK-cells in the spleen (B,C) or liver (D,E) 1 day after L.m. infection. (F) Representative flow plots of IFN-γ producing NK-cells. The frequency or number of IFN-γ+ NK-cells in the spleen (G,H) or liver (I,J). (K) Experimental Design: 2 days after surgery splenocytes from both groups of mice were harvested and stimulated with rIL-12 and rIL-18 or left unstimulated for 8 hrs. BFA was added during the last 4 hrs and intracellular cytokine production was evaluated. (L) Representative flow plots of IFN-γ producing NK-cells. (M) The frequency of IFN-γ+ NK-cells from Sham or CLP hosts in either unstimulated or stimulated wells. Data are representative from 2 independent experiments with 3–5 mice per group. Numbers above bars show fold change between groups. * p<0.05. Error bars represent the standard error of the mean.