ω-3 fatty acids suppress inflammatory cytokine production by macrophages and hepatocytes

Wu, Hao; Wong, Otto; Liu, Xuelai; Lee, Puiyan; Chen, Yan; Wong, Kenneth K.

doi:10.1016/j.jpedsurg.2010.08.044

Cited by 66 publications

(55 citation statements)

References 37 publications

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“…The general paradigm is that EPA and DHA are immunosuppressive, anti-infl ammatory, or infl ammation-resolving molecules based on studies with macrophages, neutrophils, dendritic cells, and T cells in varying model systems ( 8,(27)(28)(29)(30)(31)(32). Our lab initially identifi ed immuneenhancing properties of n-3 PUFA-enriched fi sh oil on B-cell activity in lean mice, which was recently confi rmed by others ( 11,13 ).…”

Section: Epa and Dha Ethyl Esters Differentially Promote The Moleculamentioning

confidence: 80%

Eicosapentaenoic and docosahexaenoic acid ethyl esters differentially enhance B-cell activity in murine obesity

Teague

Harris

Fenton

et al. 2014

Journal of Lipid Research

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Section: Epa and Dha Ethyl Esters Differentially Promote The Moleculamentioning

confidence: 80%

Eicosapentaenoic and docosahexaenoic acid ethyl esters differentially enhance B-cell activity in murine obesity

Teague

Harris

Fenton

et al. 2014

Journal of Lipid Research

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“…In this sense, EPA is able to prevent LPS-induced increase in TNF expression in both liver cells alone or in liver cells cocultured with macrophages (Hao et al 2010), and LPS directly inhibits Igf1 expression in hepatocyte cultures and in cocultures with Kuppfer cells (Priego et al 2006, Granado et al 2008. Furthermore, EPA induces cell proliferation in primary hepatocyte cultures (Liu et al 2011), and IGF1 has been reported to be an important factor in proliferation and in the response to damage in liver cell (Gatto et al 2008).…”

Section: Discussionmentioning

confidence: 98%

Comparison of the effects of the n-3 polyunsaturated fatty acid eicosapentaenoic and fenofibrate on the inhibitory effect of arthritis on IGF1

Castillero

López-Menduiña²,

Martín³

et al. 2011

Journal of Endocrinology

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Adjuvant-induced arthritis is a chronic inflammatory illness that induces muscle wasting and decreases circulating IGF1. Eicosapentaenoic acid (EPA) and fenofibrate, a peroxisome proliferator-activated receptors a agonist, have anti-inflammatory actions and ameliorate muscle wasting in arthritic rats. The aim of this work was to elucidate whether EPA and fenofibrate administration are able to prevent the effect of arthritis on the IGF1-IGFBP system. On day 4 after adjuvant injection control, arthritic rats were gavaged with EPA (1 g/kg) or fenofibrate (300 mg/kg) until day 15 when all rats were killed. Arthritis decreased body weight gain, serum IGF1, and liver Igf1 mRNA, whereas it increased gastrocnemius Igfbp3 mRNA. EPA, but not fenofibrate, administration prevented arthritis-induced decrease in serum IGF1 and liver Igf1 mRNA. In the rats treated with EPA arthritis increased Igfbp5 mRNA in the gastrocnemius. Fenofibrate treatment decreased IGF1 and Igf1 mRNA in the liver and gastrocnemius. In arthritic rats, fenofibrate increased body weight gain and decreased gastrocnemius Igfbp3 and Igfbp5 mRNA. These data suggest that the mechanisms through which EPA and fenofibrate act on the IGF1 system and ameliorate muscle wasting in arthritic rats are different. EPA administration increased circulating levels of IGF1, whereas fenofibrate decreased the Igfbp3 and Igfbp5 in the gastrocnemius muscle.

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“…Several studies have shown that DHA and EPA can exert antiinflammatory activities, and their beneficial effects are commonly ascribed to this property (see [34,35]). In vitro studies have shown a suppressing effect by EPA on inflammatory cytokine production in human macrophages [36], and DHA has been shown to downregulate inflammatory proteins in vitro [37] and in vivo. Dietary supplementation with DHA-rich ω3 FAs resulted in increased plasma concentrations of DHA (and EPA) in AD patients, and this was associated with reduced release of interleukin (IL)-1␤, IL-6, and granulocyte colony-stimulating factor from peripheral blood mononuclear cells ex vivo [39].…”

Section: Introductionmentioning

confidence: 99%

Omega-3 Fatty Acids Enhance Phagocytosis of Alzheimer's Disease-Related Amyloid-β42 by Human Microglia and Decrease Inflammatory Markers

Hjorth

Zhu

Toro

et al. 2013

JAD

203

154

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Abstract. The use of supplements with omega-3 (ω3) fatty acids (FAs) such as docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) is widespread due to proposed beneficial effects on the nervous and cardiovascular systems. Many effects of ω3 FAs are believed to be caused by down-regulation and resolution of inflammation. Alzheimer's disease (AD) is associated with inflammation mediated by microglia and astrocytes, and ω3 FAs have been proposed as potential treatments for AD. The focus of the present study is on the effects of DHA and EPA on microglial phagocytosis of the AD pathogen amyloid-␤ (A␤), on secreted and cellular markers of immune activity, and on production of brain-derived neurotrophic factor (BDNF). Human CHME3 microglial cells were exposed to DHA or EPA, with or without the presence of A␤ 42 . Phagocytosis of A␤ 42 was analyzed by flow cytometry in conjunction with immunocytochemistry using antibodies to cellular proteins. Secreted proteins were analyzed by ELISA. Both DHA and EPA were found to stimulate microglial phagocytosis of A␤ 42 . Phagocytosis of A␤ 42 was performed by microglia with a predominance of M2 markers. EPA increased the levels of BDNF in the culture medium. The levels of TNF-␣ were decreased by DHA. Both DHA and EPA decreased the pro-inflammatory M1 markers CD40 and CD86, and DHA had a stimulatory effect on the anti-inflammatory M2 marker CD206. DHA and EPA can be beneficial in AD by enhancing removal of A␤ 42 , increasing neurotrophin production, decreasing pro-inflammatory cytokine production, and by inducing a shift in phenotype away from pro-inflammatory M1 activation.

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ω-3 fatty acids suppress inflammatory cytokine production by macrophages and hepatocytes

Abstract: The addition of ω-3 fatty acids in TPN suppresses the inflammatory response via direct and indirect routes. The findings may help explain the clinical benefits of EPA in pediatric patients receiving long-term TPN.

Cited by 66 publications

References 37 publications

Eicosapentaenoic and docosahexaenoic acid ethyl esters differentially enhance B-cell activity in murine obesity

Eicosapentaenoic and docosahexaenoic acid ethyl esters differentially enhance B-cell activity in murine obesity

Comparison of the effects of the n-3 polyunsaturated fatty acid eicosapentaenoic and fenofibrate on the inhibitory effect of arthritis on IGF1

Omega-3 Fatty Acids Enhance Phagocytosis of Alzheimer's Disease-Related Amyloid-β42 by Human Microglia and Decrease Inflammatory Markers

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