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. Author manuscript; available in PMC: 2017 Mar 2.
Published in final edited form as: Semin Immunol. 2016 Oct 19;28(5):417–424. doi: 10.1016/j.smim.2016.10.004

Figure 3. Nitric oxide in the suppression of macrophage mitochondrial respiration.

Figure 3

(A, B) Kinetic gene expression of iNOS and arginase 1 (Arg1) in BMDMs (red bars) and pMACs (blue bars) illustrates delayed induction of iNOS and higher expression of Arg1 in pMACs. (C) Consistent with increased arginase activity, pMACs demonstrate a significant increase in ornithine production upon LPS activation. (D) This profile suggests a model in which arginine metabolism favors iNOS in BMDMs and Arg1 in pMACs. The net effect of this shift is to reduce NO release and increased mitochondrial respiration in LPS stimulated pMACs, whereas high level NO production in BMDMs suppresses mitochondrial function.