The DOI matches its Crossref record; 8 of the 8 references it cites were found in a registry or an index.
Saturated fatty acids activate TLR-mediated proinflammatory signaling pathways
Open accessAbstract
Toll-like receptor 4 (TLR4) and TLR2 were shown to be activated by saturated fatty acids (SFAs) but inhibited by docosahexaenoic acid (DHA). However, one report suggested that SFA-induced TLR activation in cell culture systems is due to contaminants in BSA used for solubilizing fatty acids. This report raised doubt about proinflammatory effects of SFAs. Our studies herein demonstrate that sodium palmitate (C16:0) or laurate (C12:0) without BSA solubilization induced phosphorylation of inhibitor of nuclear factor-κB α, c-Jun N-terminal kinase (JNK), p44/42 mitogen-activated-kinase (ERK), and nuclear factor-κB subunit p65, and TLR target gene expression in THP1 monocytes or RAW264.7 macrophages, respectively, when cultured in low FBS (0.25%) medium. C12:0 induced NFκB activation through TLR2 dimerized with TLR1 or TLR6, and through TLR4. Because BSA was not used in these experiments, contaminants in BSA have no relevance. Unlike in suspension cells (THP-1), BSA-solubilized C16:0 instead of sodium C16:0 is required to induce TLR target gene expression in adherent cells (RAW264.7). C16:0-BSA transactivated TLR2 dimerized with TLR1 or TLR6 and through TLR4 as seen with C12:0. These results and additional studies with the LPS sequester polymixin B and in MyD88(-/-) macrophages indicated that SFA-induced activation of TLR2 or TLR4 is a fatty acid-specific effect, but not due to contaminants in BSA or fatty acid preparations.
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Cites
TLR4 links innate immunity and fatty acid-induced insulin resistance
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Self-citationNutrient sensing and inflammation in metabolic diseases
Hotamisligil, G. S., & Erbay, E. (2008) · Nature Reviews Immunology · doi:10.1038/nri2449 · Cited by 1,040
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Kleinridders, A., Schenten, D., Könner, A. C., Belgardt, B. F., Mauer, J., Okamura, T., Wunderlich, F. T., Medzhitov, R., & Brüning, J. C. (2009) · Cell Metabolism · doi:10.1016/j.cmet.2009.08.013 · Cited by 483
Tlr-4 deficiency selectively protects against obesity induced by diets high in saturated fat
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“animal models of mutated or deleted TLR4 or TLR2 subsequently demonstrated that saturated fatty acids indeed can activate TLR4- and TLR2-mediated pro-inflammatory signaling pathways and consequently, increase risk of insulin resistance (10-19).”
Background
Cited by
Inflammaging: a new immune–metabolic viewpoint for age-related diseases
Franceschi, C., Garagnani, P., Parini, P., Giuliani, C., & Santoro, A. (2018) · Nature Reviews Endocrinology · doi:10.1038/s41574-018-0059-4 · Cited by 3,586
Inflammation, metaflammation and immunometabolic disorders
Hotamisligil, G. S. (2017) · Nature · doi:10.1038/nature21363 · Cited by 2,570
Oliphant, K., & Allen-Vercoe, E. (2019) · Microbiome · doi:10.1186/s40168-019-0704-8 · Cited by 1,327
Caesar, R., Tremaroli, V., Kovatcheva-Datchary, P., Cani, P. D., & Bäckhed, F. (2015) · Cell Metabolism · doi:10.1016/j.cmet.2015.07.026 · Cited by 960
Food, immunity, and the microbiome
Tilg, H., & Moschen, A. R. (2015) · Gastroenterology · doi:10.1053/j.gastro.2014.12.036 · Cited by 292
Metadata
- Authors
- Huang, S., Rutkowsky, J. M., Snodgrass, R. G., Ono-Moore, K. D., Schneider, D. A., Newman, J. W., Adams, S. H., & Hwang, D. H.
- Venue
- Journal of Lipid Research
- Publisher
- Elsevier BV
- Published
- 2012-09
- Volume
- 53
- Issue
- 9
- Pages
- 2002-2013
- ISSN
- 0022-2275 (ISSN-L)
- OpenAlex
- W2070197168
- Cited by
- 592
- References
- 8
- FWCI
- 14.54
- Type
- journal article
- Language
- en
- Open access
- hybrid
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- Huang, S., Rutkowsky, J. M., Snodgrass, R. G., Ono-Moore, K. D., Schneider, D. A., Newman, J. W., Adams, S. H., & Hwang, D. H. (2012). Saturated fatty acids activate TLR-mediated proinflammatory signaling pathways. Journal of Lipid Research. https://doi.org/10.1194/jlr.d029546
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