The suppression of eicosanoid synthesis by peritoneal macrophages is influenced by the ratio of dietary docosahexaenoic acid to linoleic acid

Lokesh, Belur R.; Black, J. Mark; Kinsella, John E.

doi:10.1007/bf02535074

Cited by 25 publications

(16 citation statements)

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“…Calif., USA) for 7 days and then randomized by weight into 4 groups of 6 animals each. The animals were then fed the experimental diets for 2 weeks prior to sacrifice, be cause this was a sufficient time to alter macrophage fatty acids [12], The experimental diets were prepared immediately prior to the start of the experimental trial by first mixing the fat-free diet with powdered tripalmitin (Sigma Chemical Company, St. Louis. Mo., USA).…”

Section: Animalsmentioning

confidence: 99%

“…Calif.. USA). Fatty acid methyl esters were identified by retention time compared to authentic standards as described [17] and quantified using pentadecanoic acid as an internal standard [ 12],…”

Section: Fatly Acid a Nalysismentioning

confidence: 99%

“…The lipids were extracted from washed PEC mac rophages (2 X I06) using the procedure of Bligh and Dyer [16], and the PL were separated by thin-layer chromatography using 80:10 chloroform:mcthanol [ 12], After saponification, the methyl esters of the fatty acids were prepared and analyzed by gas chromatogra phy using a 0.25 mm X 30 m DB-23 column (J&W Scientific. Folsom.…”

Section: Fatly Acid a Nalysismentioning

confidence: 99%

“…[8], increasing the synthesis of membrane-bound tumor necrosis factor and interleukin-1 and in some cases enhancing the release of tumor necrosis factor [9,10], However, in other studies, dietary n-3 PUFA decreased tumor necrosis factor levels in humans [11], Few studies have examined the effects of increasing dietary n-3 PUFA on macrophage function while keeping dietary n-6 PUFA constant. Lokesh et al [12] observed that increasing the ratio dietary docosahexaenoic acid to linoleic acid decreased the amount of AA released from murine resident peritoneal macrophage membrane phospholipids (PL) with concomitant decreases in macrophage synthesis of eicosanoids (PGEi, 6-keto-prostaglandin Fi", and leukotriene B4). Whelan et al [13] reported reductions in leukotriene synthesis from AA but increased synthesis of leukotrienes from eicosapentaenoic acid in zymosan-stimulated peritoneal macrophages from mice fed increasing amounts of dietary n-3 PUFA.…”

Section: Introductionmentioning

confidence: 99%

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Dietary n-3 Fatty Acids Alter Murine Peritoneal Macrophage Cytotoxicity

Je²

1993

Ann Nutr Metab

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Male CD-I mice were fed diets containing 10 wt% fat composed of a constant amount of n-6 polyunsaturated fatty acids (PUFA; safflower oil, 1.5 wt%) and increasing levels of n-3 PUFA (up to 1.5 wt%); the remaining fat was a 50:50 mixture of tripalmitin and triolein. Four days prior to sacrifice, the animals were injected intraperitoneally with sterile thioglycollate. Peritoneal macrophages were analyzed for phospholipid fatty acids, prostaglandin E₂ (PGE₂) synthesis and cytotoxicity towards L929 target cells. Increasing dietary n-3 PUFA increased macrophage phospholipid n-3 PUFA from 4.4 to 11.0 mol% with a concomitant decline in n-6 PUFA from 15.5 to 10.9 mol%, and PGE₂ synthesis declined from 2.6 to 1.5 pmol/million cells in thioglycollate-elicited macrophages. Macrophage cytotoxicity toward target L929 cells declined by approximately 50% with increasing n-3 PUFA concentration.

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Section: Animalsmentioning

confidence: 99%

Section: Fatly Acid a Nalysismentioning

confidence: 99%

Section: Fatly Acid a Nalysismentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Dietary n-3 Fatty Acids Alter Murine Peritoneal Macrophage Cytotoxicity

Je²

1993

Ann Nutr Metab

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“…Notwithstanding the homeostasis, the making in fatty acids of platelet PLs is affected by the diet, by the ratio between fatty acids saturated or not present in PPs, by their absolute dose up taken daily, and type of EFA (n-6 or n-3) mainly represented [23,24].…”

Section: Introductionmentioning

confidence: 99%

Assessment of the Essential Fatty Acids in Neonates at Risk for Atopy

Cantani¹

2015

J Biomol Res Ther

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Essential fatty acids (EFA) are the major components of cellular phospholipids (PLs), contributing to their stability and functions. They are also precursors of inflammation mediators such as prostaglandins and leukotrienes, and are involved in cellular immunoregulation.Most recent studies have stressed that EFA levels are important in various diseases. Several Authors have stated that patients with atopic dermatitis (AD) have altered EFA levels in plasmatic PLs, and showed clinical improvement after oral EFA administration. The aim of our work was to study EFA composition of PLs of cord blood lymphocytes in 32 newborns at risk for atopy, in order to correlate EFA levels at birth with total IgE values and with the onset of atopic disease. Thirty not at risk newborns were studied as controls.Our results demonstrate a significant decrease (p<0.0001) of arachidonic acid (AA) levels in lymphocytes of newborns at risk for atopy, compared to controls, whereas a not significant increase of linoleic acid (LA) was present. No reverse correlation between IgE values and AA levels was found, whereas the 6 month and 1 year follow-up have not shown any major alteration of total IgE values, on the contrary a normalization of AA levels in all but one child has been observed. Only this one child has developed AD. We stress that the preventive action on allergy development recognized to breast milk could be also due to its effect on the EFA composition of the PLs of cell membrane.

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Effects of in vitro exposure to arachidonic acid on TNF-α production by murine peritoneal macrophages

Hubbard

Lim

Somers

et al. 1993

Journal of Leukocyte Biology

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Modifying the fatty acid composition of macrophages through diet can significantly alter some of their functions, such as tumoricidal capacity and tumor necrosis factor alpha (TNF-alpha) production. The mechanism of that modification, however, is unknown. In this report, we provide evidence that fatty acids added to macrophages in culture can significantly alter macrophage TNF-alpha production. For example when inflammatory macrophages were incubated with various doses of arachidonic acid [20:4(n-6)] during activation with lipopolysaccharide (LPS), we observed a dose-dependent decrease in the level of bioactive TNF-alpha with complete inhibition at 2-5 microM. This inhibition was specific for 20:4(n-6) because in vitro treatment with other fatty acids, such as eicosapentaenoic [20:5(n-3)] or docosahexaenoic [22:6(n-3)] acids, had differential effects. The inhibitory action of 20:4(n-6) did not involve toxicity because cell viability was not affected and in vitro interferon-gamma and lipopolysaccharide (LPS) activation of macrophages for killing of P815 tumor targets was not altered. Inhibition by 20:4(n-6) occurred posttranscriptionally, and could be reversed when macrophages were treated with indomethacin during activation. Arachidonic acid treatment also significantly increased the production of immunoreactive prostaglandin E2 (PGE2) by LPS-treated and untreated macrophages. These results suggest that in vitro treatment of macrophages with 20:4(n-6) may inhibit TNF-alpha production through an alteration in the levels of PGE2 at a posttranscriptional level. These results provide evidence that some dietary fats may affect macrophage activity through modification of eicosanoid synthesis.

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The suppression of eicosanoid synthesis by peritoneal macrophages is influenced by the ratio of dietary docosahexaenoic acid to linoleic acid

Cited by 25 publications

References 25 publications

Dietary n-3 Fatty Acids Alter Murine Peritoneal Macrophage Cytotoxicity

Dietary n-3 Fatty Acids Alter Murine Peritoneal Macrophage Cytotoxicity

Assessment of the Essential Fatty Acids in Neonates at Risk for Atopy

Effects of in vitro exposure to arachidonic acid on TNF-α production by murine peritoneal macrophages

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