Metabolic shifts in immunity and inflammation

Abstract

Sites of ongoing inflammation and triggered immune responses are characterized by significant changes in metabolic activity. Recent studies have indicated that such shifts in tissue metabolism result from a combination of profound recruitment of inflammatory cells (neutrophils and monocytes) and high proliferation rates among lymphocyte populations. The resultant shifts in energy supply and demand can result in metabolic acidosis and diminished delivery and/or availability of oxygen, leading to hypoxia extensive enough to trigger transcriptional and translation changes in tissue phenotype. Such phenotypic shifts can imprint fundamental changes to tissue metabolism. In this study, we review recent work addressing metabolic changes and metabolic control of inflammation and immunity.

Figure 1. Metabolic stress points in inflammation and immunity

Migration of inflammatory cells to sites of infection changes local tissue metabolism in fundamental ways. A number of metabolic limitations contribute to substantial a shift in tissue metabolism (A). In vivo evidence for inflammation-associated hypoxia (so called “inflammatory hypoxia”) using nitroimidazole-based dye retention in vehicle treated mouse colon revealing a degree of “physiological hypoxia” (B) compared to TNBS-induced colitis resulting in intense and deep tissue hypoxia (C). (Adapted from reference , DC=dendritic cell; T=T-cell; PMN=neutrophil).