Toll-like Receptor Agonists Promote Prolonged Triglyceride Storage in Macrophages
Open accessAbstract
Macrophages in infected tissues may sense microbial molecules that significantly alter their metabolism. In a seeming paradox, these critical host defense cells often respond by increasing glucose catabolism while simultaneously storing fatty acids (FA) as triglycerides (TAG) in lipid droplets. We used a load-chase strategy to study the mechanisms that promote long term retention of TAG in murine and human macrophages. Toll-like receptor (TLR)1/2, TLR3, and TLR4 agonists all induced the cells to retain TAG for ≥3 days. Prolonged TAG retention was accompanied by the following: (a) enhanced FA uptake and FA incorporation into TAG, with long lasting increases in acyl-CoA synthetase long 1 (ACSL1) and diacylglycerol acyltransferase-2 (DGAT2), and (b) decreases in lipolysis and FA β-oxidation that paralleled a prolonged drop in adipose triglyceride lipase (ATGL). TLR agonist-induced TAG storage is a multifaceted process that persists long after most early pro-inflammatory responses have subsided and may contribute to the formation of "lipid-laden" macrophages in infected tissues.
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Lipid droplets form in myeloid cells through upregulation of lipid-synthesis enzymes triggered by engagement of toll receptors by innate immune triggers such as bacteria.
“LDs form in myeloid cells through the upregulation of lipid-synthesis enzymes triggered by the engagement of toll receptors by innate immune triggers, such as bacteria7.”
From APOE4/4 is linked to damaging lipid droplets in Alzheimer’s disease microglia (2024) · cites this paper as [7]
The Discussion reports that TLR agonists increased triglyceride synthesis and the abundance of ACSL1 and DGAT2 in macrophages, supporting the proposed link to lipid droplets. But it describes enzyme upregulation as one part of a multifaceted storage response, alongside increased fatty-acid uptake and decreased lipolysis; it does not establish this as the mechanism across myeloid cells generally. Page numbers are unavailable in our copy. (LLM, conf=0.84)
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- Authors
- Huang, Y.-L., Morales-Rosado, J., Ray, J., Myers, T. G., Kho, T., Lu, M., & Munford, R. S.
- Affiliations
- National Institutes of Health (US)
- Corresponding author
- Munford, Robert S.
- Venue
- Journal of Biological Chemistry
- Publisher
- Elsevier BV
- Published
- 2014-01
- Volume
- 289
- Issue
- 5
- Pages
- 3001-3012
- ISSN
- 0021-9258 (ISSN-L)
- PMC
- PMC3908431
- OpenAlex
- W1997812608
- Cited by
- 133
- References
- 34
- Citations by year
- 2026: 11 · 2025: 13 · 2024: 11 · 2023: 8 · 2022: 10 · 2021: 21 · 2020: 20 · 2019: 8 · 2018: 8 · 2017: 6 · 2016: 9 · 2015: 3 · 2014: 4
- FWCI
- 2.49
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Biological Chemistry (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health
- National Institute of Allergy and Infectious Diseases
- NHLBI Division of Intramural Research
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Lipid metabolism and biosynthesis
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipid metabolism and disorders
- Keywords
- TLR agonists, macrophages, triglyceride storage, lipid droplets, fatty acid uptake, diacylglycerol acyltransferase 2, adipose triglyceride lipase, lipolysis, fatty acid beta-oxidation, TLR1/2, TLR3, TLR4, lipid-laden macrophages, infection
- MeSH terms
- Animals, Cells, Cultured, Coenzyme A Ligases, Fatty Acids, Foam Cells, Humans, Lipolysis, Lipopolysaccharides, Macrophages, Mice, Inbred C57BL, Monocytes, Triglycerides, Mice, Knockout, Diacylglycerol O-Acyltransferase, Toll-Like Receptor 1, Toll-Like Receptor 2, Toll-Like Receptor 3, Toll-Like Receptor 4, Mice
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