Figure 7.

mAb-induced IL-10 works to counteract TNF-α produced by macrophages. A, IL-10–KO mice infected intravenously with 1×10⁸ CFU Acinetobacter baumannii HUMC1 and treated with 20 μg mAb were able to survive if they were depleted of macrophages or treated with an anti–TNF-α antibody (n = 5 mice per group intact and 6 mice per group macrophage depleted); *P < .05 compared to intact IL-10–KO mice. Blood was harvested at 7 hours postinfection to quantify bacterial burden in the blood and obtain plasma cytokine levels by multiplex Luminex assay. B, Bacterial burden was no different between IL-10–KO mice with an intact immune system and with macrophages depleted; however, all intact mice died and nearly all macrophage-depleted mice survived (n = 5 mice per group). C, Cytokines showed that IL-10–KO mice depleted of macrophages had near-baseline levels of TNF-α and relatively low levels of proinflammatory IL-1β and IL-6 compared to intact IL-10–KO mice (n = 5 mice per group). B and C, Plots show medians and interquartile range. Abbreviations: CFU, colony-forming unit; IL, interleukin; KO, knockout; mAb, monoclonal antibody; Mac, macrophage depleted TNF-α, tumor necrosis factor-α.