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Panezai, J.; Van Dyke, T. Polyunsaturated Fatty Acids in Immunity and Inflammation. Encyclopedia. Available online: https://encyclopedia.pub/entry/43596 (accessed on 17 July 2025).
Panezai J, Van Dyke T. Polyunsaturated Fatty Acids in Immunity and Inflammation. Encyclopedia. Available at: https://encyclopedia.pub/entry/43596. Accessed July 17, 2025.
Panezai, Jeneen, Thomas Van Dyke. "Polyunsaturated Fatty Acids in Immunity and Inflammation" Encyclopedia, https://encyclopedia.pub/entry/43596 (accessed July 17, 2025).
Panezai, J., & Van Dyke, T. (2023, April 28). Polyunsaturated Fatty Acids in Immunity and Inflammation. In Encyclopedia. https://encyclopedia.pub/entry/43596
Panezai, Jeneen and Thomas Van Dyke. "Polyunsaturated Fatty Acids in Immunity and Inflammation." Encyclopedia. Web. 28 April, 2023.
Polyunsaturated Fatty Acids in Immunity and Inflammation
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This entry is adapted from the peer-reviewed paper 10.3390/nu15040821

Polyunsaturated fatty acids (PUFAs) are a diverse set of molecules with remarkable contributions to human physiology. They not only serve as sources of fuel but also cellular structural components as well as substrates that provide bioactive metabolites. A growing body of evidence demonstrates their role in inflammation. Inflammation in the presence of a polymicrobial biofilm contributes to the pathology of periodontitis. The role PUFAs in modulating immuno-inflammatory reactions in periodontitis is only beginning to be uncovered as research continues to unravel their far-reaching immunologic implications.

fatty acids periodontitis inflammation

1. N−6 Fatty Acids

The n−6 FAs are structural components of membranes and determine membrane fluidity, signal transduction as well as the expression of cellular receptors. Their biochemical function as precursors of eicosanoids is crucial as eicosanoids are considered to be locally acting hormones that are involved in the modulation of renal and pulmonary functions, vascular tone and inflammation. The cytochrome P−450 metabolites (EETs, DiHETEs and HETEs) are important paracrine factors and second messengers with regulatory functions in pulmonary, cardiac, renal, and vascular systems as well as modulating inflammatory and growth responses, whereas LXA4 and LXB4 are potent anti-inflammatory mediators [1]. Studies have shown that increasing dietary intake of n−6 FAs results not only in increased incorporation of AA into inflammatory cells, but also the production of inflammatory eicosanoids [2][3].
A diet comprised of high n−6 FAs and low n−3 FAs i.e., a higher n−6/3 ratio, appears to lower immune cell function [4]. This effect is undesirable in many ways as long-term effects can result in lower immunity. Currently, the n−6/3 ratio in a typical Western diet is 20-fold higher than what it was hundred years ago [5]. As we know, a high n−6 FA diet leads to increased incorporation of AA in immune cell membranes. In neutrophils, monocytes and lymphocytes, almost 20% of the membranous FAs are AA as opposed to just 1% EPA and 2.5% DHA [6]. The high AA content ensures an increased supply of its metabolites; the pro-inflammatory eicosanoids, which can predispose our bodies to supra-physiologic inflammatory responses and eventually perpetuate low-grade inflammation [7]. However, n−6 FA does remain an essential requirement for the growth and maintenance of immune cells and tissues. An abundance of in vitro evidence exists for the role of AA metabolites and their regulatory role in immune cell development and functions, including monocyte growth and differentiation, Th1 and Th2 cytokine regulation, T cell proliferation and migration, antigen-presenting cell functions and macrophage TNF-α and IL−1regulation [8][9][10][11][12][13]. Also, lymphocytes preferentially incorporate n−6 fatty acids during growth and proliferation in vitro. This can be explained by the fact that the mounting of an immune response requires increased cell proliferation in the lymph nodes, which in turn would demand an increased amount of PUFA. [14]. AA derived prostanoids, especially PGE2, influence T cell activation depending on its concentration. At low concentrations, it inhibits T cell activation and differentiation, whereas at high concentrations, PGE2 enhances T cell proliferation [15]. PGD2 also exerts different effects but these are not concentration-dependent; rather receptor (type) dependent. PGD2 engages with both DP1 and DP2 receptors. Engaging with DP1 promotes T cell apoptosis while DP2 delays Th2 apoptosis [16]. Studies examining the role of TXA2 in human T lymphocytes revealed an inhibitory effect on T cell proliferation and cytokine production [17]. Leukotrienes LTD4 and LTE4 on the other hand are known to enhance Th2 cell activation and cytokine production. This effect is further amplified in the presence of fellow eicosanoid PGD2 [18]. The AA derived pro-resolving lipoxins play an important role in T-cell mediated inflammation as well. Aspirin-triggered LXA4 and LXB4 inhibit production of TNFα in anti-CD3 antibody stimulated T lymphocytes [19].
Based on several lines of evidence, n−6 FAs are considered pro-inflammatory. These include the membrane AA and its oxygenated products, the association of plasma n−6 FA levels with certain inflammatory diseases and augmented autoimmunity in certain diseases [20]. Non-metabolized AA alone is capable of exerting direct effects on cell membranes as seen in its involvement in the production of reactive oxygen species (ROS), partly via NADPH oxidase NOX−2 which is located in the plasma membrane [21][22]. Non-metabolized AA can also alter the mechanical properties of the bilayer, thereby modulating the function of membrane channels and perturbing the localization of transmembrane receptors [23][24].
Paradoxically, the n−6 FAs have demonstrated protective effects in immune-mediated inflammatory diseases. An interesting finding has highlighted AA’s role in preventing pro-inflammatory signaling cascades indirectly [24]. Zhang et al. discovered that AA not only prevented the TLR4 complex formation with accessory proteins which is induced by saturated fatty acid but also the induction of pro-inflammatory cytokines in cultured cardiomyocytes and macrophages. This was due to AA’s ability to directly bind to TLR4 co-receptor, myeloid differentiation factor 2 (MD2) which prevented saturated fatty acids from activating TLR4 pro-inflammatory signaling pathway [24].
The anti-inflammatory effects n−6 FAs are similar to n−3 FAs and have been observed in other studies where n−6 FAs induced the production of nuclear transcription factors, enzymes, and cytokines in human cells [25]. Similar to the effects of DHA and EPA, GLA enhanced levels of the transcription factor peroxisome proliferator-activated receptor-gamma (PPAR-γ), which propagates anti-inflammatory effects decreased production of pro-inflammatory cytokines including interleukins (IL) 6 and 8 [25].

2. N−3 Fatty Acids and SPMs

Increased consumption of n−3 FAs, including EPA and DHA, results in increased proportions of those fatty acids in inflammatory cell membranes [26][27]. The incorporation of EPA and DHA into inflammatory cell membranes occurs in a dose dependent manner whilst outcompeting AA. As a result, less substrate AA becomes available for the synthesis of inflammatory eicosanoids by inflammatory cells decreasing their production of PGE2, thromboxane B2, LTB4, and LTE4 [28]. With increased availability of EPA and DHA in membranes, the inflammatory eicosanoids not only decrease, but an alternate family of mediators are produced including EPA derived eicosanoids (PGE3, LTB5), endocannabinoids, and SPMs (E-series and D-series resolvins, protectins and maresins). EPA derived eicosanoids are less biologically active than those produced from AA [29][30]. Being structurally different, the eicosanoid receptors have a lower affinity for the EPA-derived mediators [31].
With increased dietary intake of DHA, an increase in the activity of phagocytes (neutrophils and monocytes) occurs. An intake of a DHA rich fish oil (3 g per day) containing 54% DHA can increase the phagocytic activity of neutrophils and monocytes by 62% and 145% respectively [32]. These changes were not observed with EPA rich fish oil [33]. This impact on phagocytes shows DHA’s immunomodulatory strength in an acute inflammatory response. Nuclear factor kappa B (NFκB) is an important transcription factor involved in inflammatory responses. It is the main transcription factor required for up-regulating the genes encoding inflammatory cytokines, adhesion molecules as well as COX−2 [34]. When activated by extracellular inflammatory stimuli, NFκB’s inhibitory subunit (IκB) undergoes phosphorylation, which then allows translocation of the remaining NFκB dimer to the nucleus [35]. Both EPA and DHA can reduce NFκB activation in response to endotoxin in cultured macrophages and human monocytes due to decreased IκB phosphorylation [36][37].
The modulatory actions of n−3 FAs on T cells are generally suppressive in nature and specific cell responses are modulated according to the T cell subtype [38]. These suppressive actions are thought to be mediated through the perturbation of lipid rafts in the plasma membrane [39]. Lipid rafts can be defined as dynamic nanoscale domains formed via lipid-lipid and lipid-protein interactions. Incorporation of n−3 FAs in T helper cell membranes destabilizes the rafts resulting in the displacement of many signaling proteins necessary for T cell activation, including the Src family kinases Lck and Fyn [40][41][42]. Both EPA and DHA affect the motility of T cells as their membranous incorporation interferes with cytoskeletal rearrangements [43]. Furthermore, n−3 FAs increase the formation of M2 macrophages, also known as pro-resolving or regulatory macrophages, which then induce the differentiation of T cells into regulatory T cells [44].
SPMs are potent anti-inflammatory mediators which were discovered as distinct EPA- and DHA- derived mediators. They share some of the basic pro-resolving and protective actions of lipoxins with great potency in several inflammatory disease models. Distinct SPM facilitate the resolution of inflammation and accelerate tissue regeneration and tissue repair [45]. SPMs suppress the synthesis of pro-inflammatory cytokines including IL−1, IL−6, and IL−8 via down-regulation of the NFκB pathway [46]. This, in addition to halting leukocyte infiltration into inflamed tissues, distinguishes the EPA-derived resolvins (E-series resolvins), DHA-derived resolvins (D-series resolvins), and DHA-derived protectins as immunoresolving agents [46]. Maresins, also derived from DHA, stimulate phagocytosis whilst reducing neutrophil infiltration [47]. 13(S),14(S)-epoxymaresin also inhibits the production of LTB4 derived from AA through direct inactivation of the LTA4 hydrolase enzyme, which catalyzes the conversion of leukotriene A4 into the pro-inflammatory metabolite, LTB4 [48]. SPMs also promote the the return to a homeostatic milieu by removing apoptotic cellular debris from tissues and limiting the formation of free radicals [49]. The bioactions of SPMs occur within a low nanomolar range as demonstrated by in vitro and in vivo studies [50].

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