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Cited by 243Inflammasome and immune disordersImmune Response and InflammationAdipokines, Inflammation, and Metabolic Diseases

Inflammasome-Mediated Secretion of IL-1β in Human Monocytes through TLR2 Activation; Modulation by Dietary Fatty Acids

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Snodgrass, Ryan G, Huang, Shurong, Choi, Il-Whan, Rutledge, John C, Hwang, Daniel H·2013·The Journal of Immunology
DOI 10.4049/jimmunol.1300298PMC PMC3825708
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Abstract

Many studies have shown that TLR4- and TLR2-deficient mice are protected from high-fat diet–induced inflammation and insulin resistance, suggesting that saturated fatty acids derived from the high-fat diet activate TLR-mediated proinflammatory signaling pathways and induce insulin resistance. However, evidence that palmitic acid, the major dietary saturated fatty acid, can directly activate TLR has not been demonstrated. In this article, we present multiple lines of evidence showing that palmitic acid directly activates TLR2, a major TLR expressed on human monocytes, by inducing heterodimerization with TLR1 in an NADPH oxidase–dependent manner. Dimerization of TLR2 with TLR1 was inhibited by the n-3 fatty acid docosahexaenoic acid. Activation of TLR2 by palmitic acid leads to expression of pro–IL-1β that is cleaved by caspase-1, which is constitutively present in monocytes, to release mature IL-1β. Our results reveal mechanistic insight about how palmitic acid activates TLR2, upregulates NALP3 expression, and induces inflammasome-mediated IL-1β production in human monocytes, which can trigger enhanced inflammation in peripheral tissues, and suggest that these processes are dynamically modulated by the types of dietary fat we consume.

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  • Dietary palmitic acid directly activates Toll-like receptor (TLR)-2 in mouse monocytes.

    “Remarkably, dietary palmitic acid directly activates Toll-like receptor (TLR)-2 in mouse monocytes15”

    From Sebaceous-immunobiology is orchestrated by sebum lipids (2017) · cites this paper as [15]

    The Abstract and Discussion (page numbers not provided) state that palmitic acid directly activates TLR2 in human monocytes. They do not establish the citing sentence’s claim about mouse monocytes. (LLM, conf=0.90)

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Sorted by citations

Authors
Snodgrass, R. G., Huang, S., Choi, I.-W., Rutledge, J. C., & Hwang, D. H.
Affiliations
  • Agricultural Research Service (US)
  • Inje University (KR)
  • University of California, Davis (US)
Corresponding author
Huang, Shurong
ORCID
Venue
The Journal of Immunology
Publisher
Oxford University Press (OUP)
Published
2013-10
Volume
191
Issue
8
Pages
4337-4347
ISSN
  • 0022-1767 (ISSN-L)
  • 1550-6606
DOI
10.4049/jimmunol.1300298
PMC
PMC3825708
OpenAlex
W2150982739
Cited by
243
References
7
Citations by year
2026: 15 · 2025: 13 · 2024: 21 · 2023: 20 · 2022: 20 · 2021: 20 · 2020: 19 · 2019: 21 · 2018: 16 · 2017: 26 · 2016: 22 · 2015: 19 · 2014: 9 · 2013: 1
FWCI
7.62
Type
journal article
Language
en
Open access
Licence
academic.oup.com/pages/standard-publication-reuse-rights (vor)
Locations
  • The Journal of Immunology (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • National Institute on Aging (R01AG039094)
  • National Institute of Diabetes and Digestive and Kidney Diseases (R01 DK 41868, R01DK041868, R01DK078328, R01DK064007)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
  • Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
  • Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
Keywords
inflammasome, IL-1β secretion, TLR2, palmitic acid, saturated fatty acids, docosahexaenoic acid, omega-3 fatty acids, NADPH oxidase, caspase-1, NLRP3, monocytes, insulin resistance, high-fat diet, dietary fat
MeSH terms
NLR Family, Pyrin Domain-Containing 3 Protein, Carrier Proteins, Cell Line, Dietary Fats, Docosahexaenoic Acids, Enzyme Activation, Fatty Acids, Humans, Inflammation, Insulin Resistance, Monocytes, Up-Regulation, Crystallography, X-Ray, NADPH Oxidases, Dimerization, Palmitic Acid, Caspase 1, RNA Interference, RNA, Small Interfering, Toll-Like Receptor 1, Toll-Like Receptor 2, Interleukin-1beta, Protein Multimerization, Inflammasomes

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