Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2010 Apr 15;184(8):4062-8.
doi: 10.4049/jimmunol.0903002.

Metabolic shifts in immunity and inflammation

Douglas J Kominsky  1 , Eric L Campbell, Sean P Colgan
Affiliations
Review

Metabolic shifts in immunity and inflammation

Douglas J Kominsky et al. J Immunol. .

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.

PubMed Disclaimer

Conflict of interest statement

The authors declare no financial interests in any of the work submitted here.

Figures

Figure 1
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).
See this image and copyright information in PMC

References

    1. Taylor CT, Colgan SP. Hypoxia and gastrointestinal disease. J Mol Med. 2008;85:1295–1300. - PubMed
    1. Lewis JS, Lee JA, Underwood JC, Harris AL, Lewis CE. Macrophage responses to hypoxia: relevance to disease mechanisms. J Leukoc Biol. 1999;66:889–900. - PubMed
    1. Fox CJ, Hammerman PS, Thompson CB. Fuel feeds function: energy metabolism and the T-cell response. Nat Rev Immunol. 2005;5:844–852. - PubMed
    1. Sitkovsky M, Lukashev D. Regulation of immune cells by local-tissue oxygen tension: HIF1 alpha and adenosine receptors. Nat Rev Immunol. 2005;5:712–721. - PubMed
    1. van Raam BJ, Sluiter W, de Wit E, Roos D, Verhoeven AJ, Kuijpers TW. Mitochondrial membrane potential in human neutrophils is maintained by complex III activity in the absence of supercomplex organisation. PLoS One. 2008;3:e2013. - PMC - PubMed

Publication types