Fatty acid control of nitric oxide production by macrophages

Lima, Thaís Martins de; Lima, Larissa de Sá; Scavone, Cristóforo; Curi, Rui

doi:10.1016/j.febslet.2006.04.091

Cited by 46 publications

(37 citation statements)

References 62 publications

(66 reference statements)

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“…Most of them have shown that FAs inhibit NF-κB DNA-binding activity in macrophages [53,[63][64][65], and similar results have been observed by our group [66]. There is evidence, however, that saturated FAs induce NF-κB activation, and this effect may be related to the inflammatory changes observed in adipocyte and macrophage interactions [67].…”

Section: Nf-κbsupporting

confidence: 85%

Mechanisms by which fatty acids regulate leucocyte function

et al. 2007

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Fatty acids (FAs) have been shown to alter leucocyte function and thus to modulate inflammatory and immune responses. In this review, the effects of FAs on several aspects of lymphocyte, neutrophil and macrophage function are discussed. The mechanisms by which FAs modulate the production of lipid mediators, activity of intracellular signalling pathways, activity of lipid-raft-associated proteins, binding to TLRs (Toll-like receptors), control of gene expression, activation of transcription factors, induction of cell death and production of reactive oxygen and nitrogen species are described in this review. The rationale for the use of specific FAs to treat patients with impaired immune function is explained. Substantial improvement in the therapeutic usage of FAs or FA derivatives may be possible based on an improvement in the understanding of the precise molecular mechanisms of action with respect to the different leucocyte types and outcome with respect to the inflammatory responses.

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Section: Nf-κbsupporting

confidence: 85%

Mechanisms by which fatty acids regulate leucocyte function

et al. 2007

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“…Our and other studies observed a decrease in the LPS-induced production of proinflammatory cytokines and NO by monocytes and macrophages after exposure to LA [16,25]. It is noteworthy that our data showed that GLA has more potent effective than LA in modulating the production of proinflammatory mediators.…”

Section: Discussionmentioning

confidence: 44%

Gamma-Linolenic Acid Inhibits Inflammatory Responses by Regulating NF-κB and AP-1 Activation in Lipopolysaccharide-Induced RAW 264.7 Macrophages

et al. 2009

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Gamma linolenic acid (GLA) is a member of the n-6 family of polyunsaturated fatty acids and can be synthesized from linoleic acid (LA) by the enzyme delta-6-desaturase. The therapeutic values of GLA supplementation have been documented, but the molecular mechanism behind the action of GLA in health benefits is not clear. In this study, we assessed the effect of GLA with that of LA on lipopolysaccharide (LPS)-induced inflammatory responses and further explored the molecular mechanism underlying the pharmacological properties of GLA in mouse RAW 264.7 macrophages. GLA significantly inhibited LPS-induced protein expression of inducible nitric oxide synthase, pro-interleukin-1beta, and cyclooxygenase-2 as well as nitric oxide production and the intracellular glutathione level. LA was less potent than GLA in inhibiting LPS-induced inflammatory mediators. Both GLA and LA treatments dramatically inhibited LPS-induced IkappaB-alpha degradation, IkappaB-alpha phosphorylation, and nuclear p65 protein expression. Moreover, LPS-induced nuclear factor-kappaB (NF-kappaB) and activator protein-1 (AP-1) nuclear protein-DNA binding affinity and reporter gene activity were significantly decreased by LA and GLA. Exogenous addition of GLA but not LA significantly reduced LPS-induced expression of phosphorylated extracellular signal-regulated kinase (ERK) 1/2 and c-Jun N-terminal kinase (JNK)-1. Our data suggest that GLA inhibits inflammatory responses through inactivation of NF-kappaB and AP-1 by suppressed oxidative stress and signal transduction pathway of ERK and JNK in LPS-induced RAW 264.7 macrophages.

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“…Research from the last 30 years has shown that fatty acids (FAs), despite their simple structure, can modulate many macrophage functions, including adhesion and phagocyte capacity [1,2], production of reactive oxygen and nitrogen species [3][4][5] and cytokine release [6][7][8][9]. Among the cytokine modulated by FA, tumor necrosis factor (TNF-a) is of great interest due to its role in the inflammation process observed in several diseases such as rheumatoid arthritis, atherosclerosis, and obesity [10][11][12].…”

Section: Introductionmentioning

confidence: 99%

Molecular Mechanisms by Which Saturated Fatty Acids Modulate TNF-α Expression in Mouse Macrophage Lineage

Lima-Salgado

Alba-Loureiro

Nascimento

et al. 2010

Cell Biochem Biophys

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Many macrophage functions are modulated by fatty acids (FAs), including cytokine release, such as tumor necrosis factor-α (TNF-α). TNF-α is of great interest due to its role in the inflammation process observed in several diseases such as rheumatoid arthritis, atherosclerosis, and obesity. However, the mechanisms by which FA effects occur have not been completely elucidated yet. In this study, we used a mouse monocyte lineage (J774 cells) to evaluate the effect of 50 and 100 μM of saturated (palmitic and stearic acids), monounsaturated (oleic acid) and polyunsaturated (linoleic acid) FAs on TNF-α production. Alterations in gene expression, poly(A) tail length and activation of transcription factors were evaluated. Oleic and linoleic acids, usually known as neutral or pro-inflammatory FA, inhibited LPS-induced TNF-α secretion by the cells. Saturated FAs were potent inducers of TNF-α expression and secretion under basal and inflammatory conditions (in the presence of LPS). Although the effect of the saturated FA was similar, the mechanism involved in each case seem to be distinct, as palmitic acid increased EGR-1 and CREB binding activity and stearic acid increased mRNA poly(A) tail. These results may contribute to the understanding of the molecular mechanisms by which saturated FAs modulate the inflammatory response and may lead to design of associations of dietary and pharmacological strategies to counteract the pathological effects of TNF-α.

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Fatty acid control of nitric oxide production by macrophages

Cited by 46 publications

References 62 publications

Mechanisms by which fatty acids regulate leucocyte function

Mechanisms by which fatty acids regulate leucocyte function

Gamma-Linolenic Acid Inhibits Inflammatory Responses by Regulating NF-κB and AP-1 Activation in Lipopolysaccharide-Induced RAW 264.7 Macrophages

Molecular Mechanisms by Which Saturated Fatty Acids Modulate TNF-α Expression in Mouse Macrophage Lineage

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