Alveolar macrophage immunometabolism and lung function impairment in smoking and chronic obstructive pulmonary disease

Background: Metabolic plasticity involving shifts between mitochondrial respiration and glycolysis is emerging as a crucial component of efficient innate immune cell responses. Alveolar macrophages (AMs), the most abundant antigen-presenting cells in the lung, are dramatically increased in the lungs of patients with chronic obstructive pulmonary disease (COPD). However, COPD AMs exhibit dysfunctional responses to infection with lower phagocytic ability and impairment of mitochondrial reactive oxygen species (ROS) generation. Little is known about the mitochondrial function or respiration of these cells and whether alterations in their mitochondrial or glycolytic activities may contribute to the pathogenesis of COPD.

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O'Beirne SL, Kikkers SA, Oromendia C, Salit J, Rostmai MR, Ballman KV, Kaner RJ, Crystal RG, Cloonan SM