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A Mouse Model for Pathogen-induced Chronic Inflammation at Local and Systemic Sites
Published on: August 8, 2014
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Postprandial low-grade inflammation does not specifically require TLR4 activation in the rat
Dominique Hermier1, Véronique Mathé1, Annaïg Lan1
1UMR Physiologie de la Nutrition et du Comportement Alimentaire, AgroParisTech, INRA, Université Paris-Saclay, 16 rue Claude Bernard, F-75005 Paris, France.
Nutrition & Metabolism
|October 28, 2017
Summary
Toll-like receptor 4 (TLR4) inhibition did not prevent postprandial inflammation. Instead, TLR4 and TLR2 appear to work together, influencing inflammatory responses in adipose tissue after a high-fat meal.
Area of Science:
- Immunology
- Metabolic Research
- Molecular Biology
Background:
- Innate immunity involves Toll-like receptors (TLRs), including TLR4.
- High-fat meals, particularly those rich in saturated fatty acids (SFA), are linked to postprandial inflammation.
- TLR4 is hypothesized to mediate inflammation induced by SFA-rich meals.
Purpose of the Study:
- To investigate the role of TLR4 in mediating postprandial inflammation induced by SFA-rich meals.
- To compare the effects of a TLR4 inhibitor (INH) versus a vehicle (VEH) on inflammatory markers.
- To explore the expression of inflammatory and adhesion molecules in response to SFA intake and TLR4 inhibition.
Main Methods:
- A cross-over kinetic study in rats using intravenous administration of INH or VEH before a test meal.
- Measurement of plasma inflammatory and vascular markers over 6 hours.
- Parallel study measuring mRNA levels of cytokines, TLRs, and adhesion molecules in adipose tissue, liver, and aorta.
Main Results:
- Plasma IL-6 and PAI-1 levels increased similarly after INH and VEH, indicating no specific TLR4 requirement for systemic response.
- Adipose tissue expression of TLR2 and multiple cytokine genes was significantly higher after INH.
- Liver expression of certain inflammatory genes and TLR2 was also elevated after INH, suggesting a complex interplay.
Conclusions:
- TLR4 activation is not solely required for systemic postprandial inflammation.
- TLR2 and TLR4 likely exert a dual and interdependent role in mediating postprandial inflammation, particularly in adipose tissue.
