The DOI matches its Crossref record; 21 of the 21 references it cites were found in a registry or an index.
High salt reduces the activation of IL-4– and IL-13–stimulated macrophages
Open accessAbstract
A high intake of dietary salt (NaCl) has been implicated in the development of hypertension, chronic inflammation, and autoimmune diseases. We have recently shown that salt has a proinflammatory effect and boosts the activation of Th17 cells and the activation of classical, LPS-induced macrophages (M1). Here, we examined how the activation of alternative (M2) macrophages is affected by salt. In stark contrast to Th17 cells and M1 macrophages, high salt blunted the alternative activation of BM-derived mouse macrophages stimulated with IL-4 and IL-13, M(IL-4+IL-13) macrophages. Salt-induced reduction of M(IL-4+IL-13) activation was not associated with increased polarization toward a proinflammatory M1 phenotype. In vitro, high salt decreased the ability of M(IL-4+IL-13) macrophages to suppress effector T cell proliferation. Moreover, mice fed a high salt diet exhibited reduced M2 activation following chitin injection and delayed wound healing compared with control animals. We further identified a high salt-induced reduction in glycolysis and mitochondrial metabolic output, coupled with blunted AKT and mTOR signaling, which indicates a mechanism by which NaCl inhibits full M2 macrophage activation. Collectively, this study provides evidence that high salt reduces noninflammatory innate immune cell activation and may thus lead to an overall imbalance in immune homeostasis.
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Cites
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Mosser, D. M., & Edwards, J. P. (2008) · Nature Reviews Immunology · doi:10.1038/nri2448 · Cited by 9,144
Singer, A. J., & Clark, R. A. F. (1999) · New England Journal of Medicine · doi:10.1056/nejm199909023411006 · Cited by 6,106
Obesity induces a phenotypic switch in adipose tissue macrophage polarization
Lumeng, C. N., Bodzin, J. L., & Saltiel, A. R. (2007) · Journal of Clinical Investigation · doi:10.1172/jci29881 · Cited by 4,664
Succinate is an inflammatory signal that induces IL-1β through HIF-1α
Tannahill, G. M., Curtis, A. M., Adamik, J., Palsson-McDermott, E. M., McGettrick, A. F., Goel, G., Frezza, C., Bernard, N. J., Kelly, B., Foley, N. H., et al. (2013) · Nature · doi:10.1038/nature11986 · Cited by 4,176
Functional Polarization of Tumour-Associated Macrophages by Tumour-Derived Lactic Acid
Colegio, O. R., Chu, N.-Q., Szabo, A. L., Chu, T., Rhebergen, A. M., Jairam, V., Cyrus, N., Brokowski, C. E., Eisenbarth, S. C., Phillips, G. M., et al. (2014) · Nature · doi:10.1038/nature13490 · Cited by 3,046
Transcriptome-Based Network Analysis Reveals a Spectrum Model of Human Macrophage Activation
Xue, J., Schmidt, S. V., Sander, J., Draffehn, A., Krebs, W., Quester, I., De Nardo, D., Gohel, T. D., Emde, M., Schmidleithner, L., et al. (2014) · Immunity · doi:10.1016/j.immuni.2014.01.006 · Cited by 2,210
Macrophage-specific PPARγ controls alternative activation and improves insulin resistance
Odegaard, J. I., Ricardo-Gonzalez, R. R., Goforth, M. H., Morel, C. R., Subramanian, V., Mukundan, L., Eagle, A. R., Vats, D., Brombacher, F., Ferrante, A. W., et al. (2007) · Nature · doi:10.1038/nature05894 · Cited by 2,107
Shi, L. Z., Wang, R., Huang, G., Vogel, P., Neale, G., Green, D. R., & Chi, H. (2011) · Journal of Experimental Medicine · doi:10.1084/jem.20110278 · Cited by 1,803
Large-scale association analysis identifies new risk loci for coronary artery disease
The CARDIoGRAMplusC4D Consortium, Deloukas, P., DIAGRAM Consortium, CARDIOGENICS Consortium, MuTHER Consortium, Wellcome Trust Case Control Consortium, Kanoni, S., Willenborg, C., Farrall, M., Assimes, T. L., et al. (2013) · Nature Genetics · doi:10.1038/ng.2480 · Cited by 1,614
Sodium chloride drives autoimmune disease by the induction of pathogenic TH17 cells
Kleinewietfeld, M., Manzel, A., Titze, J., Kvakan, H., Yosef, N., Linker, R. A., Muller, D. N., & Hafler, D. A. (2013) · Nature · doi:10.1038/nature11868 · Cited by 1,394
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Self-citationImpacts of microbiome metabolites on immune regulation and autoimmunity
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Metadata
- Authors
- Binger, K. J., Gebhardt, M., Heinig, M., Rintisch, C., Schroeder, A., Neuhofer, W., Hilgers, K., Manzel, A., Schwartz, C., Kleinewietfeld, M., Voelkl, J., Schatz, V., Linker, R. A., Lang, F., Voehringer, D., Wright, M. D., Hubner, N., Dechend, R., Jantsch, J., Titze, J., & Müller, D. N.
- Venue
- Journal of Clinical Investigation
- Published
- 2015-10-20
- Volume
- 125
- Issue
- 11
- Pages
- 4223-4238
- ISSN
- 0021-9738 (ISSN-L)
- 1558-8238
- OpenAlex
- W2139654366
- Cited by
- 281
- References
- 21
- FWCI
- 11.82
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Binger, K. J., Gebhardt, M., Heinig, M., Rintisch, C., Schroeder, A., Neuhofer, W., Hilgers, K., Manzel, A., Schwartz, C., Kleinewietfeld, M., Voelkl, J., Schatz, V., Linker, R. A., Lang, F., Voehringer, D., Wright, M. D., Hubner, N., Dechend, R., Jantsch, J., . . . Müller, D. N. (2015). High salt reduces the activation of IL-4– and IL-13–stimulated macrophages. Journal of Clinical Investigation. https://doi.org/10.1172/jci80919
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