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. 2015 Aug 20;13(8):5402-24.
doi: 10.3390/md13085402.

The Anti-Inflammatory Effect of Algae-Derived Lipid Extracts on Lipopolysaccharide (LPS)-Stimulated Human THP-1 Macrophages

Ruairi C Robertson  1   2 , Freddy Guihéneuf  3 , Bojlul Bahar  4 , Matthias Schmid  5 , Dagmar B Stengel  6 , Gerald F Fitzgerald  7   8 , R Paul Ross  8   9 , Catherine Stanton  10   11
Affiliations

The Anti-Inflammatory Effect of Algae-Derived Lipid Extracts on Lipopolysaccharide (LPS)-Stimulated Human THP-1 Macrophages

Ruairi C Robertson et al. Mar Drugs. .

Abstract

Algae contain a number of anti-inflammatory bioactive compounds such as omega-3 polyunsaturated fatty acids (n-3 PUFA) and chlorophyll a, hence as dietary ingredients, their extracts may be effective in chronic inflammation-linked metabolic diseases such as cardiovascular disease. In this study, anti-inflammatory potential of lipid extracts from three red seaweeds (Porphyra dioica, Palmaria palmata and Chondrus crispus) and one microalga (Pavlova lutheri) were assessed in lipopolysaccharide (LPS)-stimulated human THP-1 macrophages. Extracts contained 34%-42% total fatty acids as n-3 PUFA and 5%-7% crude extract as pigments, including chlorophyll a, β-carotene and fucoxanthin. Pretreatment of the THP-1 cells with lipid extract from P. palmata inhibited production of the pro-inflammatory cytokines interleukin (IL)-6 (p < 0.05) and IL-8 (p < 0.05) while that of P. lutheri inhibited IL-6 (p < 0.01) production. Quantitative gene expression analysis of a panel of 92 genes linked to inflammatory signaling pathway revealed down-regulation of the expression of 14 pro-inflammatory genes (TLR1, TLR2, TLR4, TLR8, TRAF5, TRAF6, TNFSF18, IL6R, IL23, CCR1, CCR4, CCL17, STAT3, MAP3K1) by the lipid extracts. The lipid extracts effectively inhibited the LPS-induced pro-inflammatory signaling pathways mediated via toll-like receptors, chemokines and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) signaling molecules. These results suggest that lipid extracts from P. lutheri, P. palmata, P. dioica and C. crispus can inhibit LPS-induced inflammatory pathways in human macrophages. Therefore, algal lipid extracts should be further explored as anti-inflammatory ingredients for chronic inflammation-linked metabolic diseases.

Keywords: THP-1; bioactive pigments; chlorophyll a; inflammation; lipids; macroalgae; macrophages; microalgae; n-3 PUFA; polyunsaturated fatty acids.

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Figures

Figure 1
Figure 1
Distribution of fatty acids within lipid classes in (A) Pavlova lutheri; (B) Palmaria palmata; (C) Porphyra dioica; (D) Chondrus crispus. * Identified using Rf values from the literature using similar migration solvent systems without using standards; " Sum of other unidentified polar lipids, i.e., phospholipids and betaine lipids; No symbol: Identified using Rf values from the literature and standards; EPA: eicosapentaenoic acid; DHA: docosahexaenoic acid; TAG: triacylglycerol; FFA: free fatty acids; DAG: diacylglycerols; MAG: monoacylglycerols; MGDG: monogalactosyldiacylglycerols; DPG: diphosphatidylacylglycerols; SG: acylated sterol glycosides; PE: phosphatidylethanolamines; PG: phosphatidylglycerols; DGDG: digalactosyldiacylglycerols; SQDG: sulfoquinovosyldiacylglycerols; PC: phosphatidylcholines; PI: phosphatidylinositols; UN: unidentified.
Figure 2
Figure 2
Effects of algal lipid extracts exposure on interleukin-6 (IL-6), IL-8 production and tumor necrosis factor α (TNFα) production in lipopolysaccharide (LPS)-stimulated THP-1 macrophages. THP-1 macrophages were exposed to the respective algae-lipid extracts or the vehicle control (dimethyl sulfoxide, DMSO) for 24 h and incubated with 100 ng·mL−1 LPS for a further 24 h. Values represent mean ± standard error (SE) normalized to DMSO control. * p ≤ 0.05; ** p ≤ 0.01.
Figure 3
Figure 3
Validation of PCR array results through quantitative PCR. Effects of algal lipid extracts exposure on expression of TLR1, TLR8, and TRAF5 genes in lipopolysaccharide (LPS)-stimulated THP-1 macrophages. * p ≤ 0.05. ** p ≤ 0.01.
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