Tissue Resident Alveolar Macrophages Do Not Rely on Glycolysis for LPS-induced Inflammation.

In this study, we show that TR-AMs rely on oxidative phosphorylation to meet their energy demands and maintain extremely low levels of glycolysis under steady-state conditions. Unlike BMDMs, TR-AMs do not experience enhanced glycolysis in response to lipopolysaccharide (LPS), and glycolytic inhibition had no effect on their proinflammatory cytokine production. HIF-1α stabilization promoted glycolysis in TR-AMs and shifted energy production away from oxidative metabolism at baseline, but it was not sufficient for TR-AMs to mount further increases in glycolysis or enhance immune function in response to LPS. Importantly, we confirmed these findings in an in vivo influenza model where infiltrating macrophages had significantly higher glycolytic and proinflammatory gene expression compared to TR-AMs. These findings demonstrate that glycolysis is dispensable for macrophage effector function in TR-AMs, and highlight the importance of macrophage tissue origin (tissue resident vs. recruited) in immunometabolism. PMID: 31469581 [PubMed - as supplied by publisher]
Source: Am J Respir Cell Mol... - Category: Respiratory Medicine Authors: Tags: Am J Respir Cell Mol Biol Source Type: research