Dietary Free Oleic and Linoleic Acid Enhances Neutrophil Function and Modulates the Inflammatory Response in Rats
Department of Physiology and Biophysics, Institute of Biomedical Sciences, São Paulo University, Avenida Prof. Lineu Prestes, 1524, Butantã, São Paulo, SP, 05508-900, Brazil. Lipids
(Impact Factor: 1.85).
09/2010; 45(9):809-19. DOI: 10.1007/s11745-010-3461-9
The high ingestion of oleic (OLA) and linoleic (LNA) acids by Western populations, the presence of inflammatory diseases in these populations, and the importance of neutrophils in the inflammatory process led us to investigate the effects of oral ingestion of unesterified OLA and LNA on rat neutrophil function. Pure OLA and LNA were administered by gavage over 10 days. The doses used (0.11, 0.22 and 0.44 g/kg of body weight) were based on the Western consumption of OLA and LNA. Neither fatty acid affected food, calorie or water intake. The fatty acids were not toxic to neutrophils as evaluated by cytometry using propidium iodide (membrane integrity and DNA fragmentation). Neutrophil migration in response to intraperitoneal injection of glycogen and in the air pouch assay, was elevated after administration of either OLA or LNA. This effect was associated with enhancement of rolling and increased release of the chemokine CINC-2alphabeta. Both fatty acids elevated L-selectin expression, whereas no effect on beta(2)-integrin expression was observed, as evaluated by flow cytometry. LNA increased the production of proinflammatory cytokines (IL-1beta and CINC-2alphabeta) by neutrophils after 4 h in culture and both fatty acids decreased the release of the same cytokines after 18 h. In conclusion, OLA and LNA modulate several functions of neutrophils and can influence the inflammatory process.
Available from: Fabio Takeo Sato
- "Oral administration of pure oleic acid (0.22 g/ kg of body weight) also induced neutrophil recruitment in a rat air-pouch model (Rodrigues et al., 2010). This effect may be explained by the enhancement in the CXCL3 release and in the neutrophil–endothelium interaction (Rodrigues et al., 2010). "
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ABSTRACT: Neutrophils are well-known to act in the destruction of invading microorganisms. They have also been implicated in the activation of other immune cells including B- and T-lymphocytes and in the resolution of inflammation and tissue regeneration. Neutrophils are produced in the bone marrow and released into the circulation from where they migrate to tissues to perform their effector functions. Neutrophils are in constant contact with fatty acids that can modulate their function, activation and fate (survival or cell death) through different mechanisms. In this review, the effects of fatty acids pertaining to five classes, namely, long-chain saturated fatty acids (LCSFAs), short-chain fatty acids (SCFAs), and omega-3 (n-3), omega-6 (n-6) and omega-9 (n-9) unsaturated fatty acids, on neutrophils and the relevance of these effects for disease development are discussed.
Copyright © 2015 Elsevier B.V. All rights reserved.
Available from: Marco Aurélio Vinolo
- "Our results showed that sunflower oil supplementation causes a clear pro-inflammatory response in mice fed on control diet and it does not have additive or prophylactic effects in mice fed on HFD. Fatty acid effects on immune system have been studied since 1970's decade . Linoleic acid is an essential fatty acid that leads to inflammatory response by increasing arachidonic acid production, a fatty acid related to elevated pro-inflammatory mediator generation . "
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ABSTRACT: High consumption of polyunsaturated fatty acids, such as sunflower oil has been associated to beneficial effects in plasma lipid profile, but its role on inflammation and insulin resistance is not fully elucidated yet. We evaluated the effect of sunflower oil supplementation on inflammatory state and insulin resistance condition in HFD-induced obese mice. C57BL/6 male mice (8 weeks) were divided in four groups: (a) control diet (CD), (b) HFD, (c) CD supplemented with n-6 (CD + n-6), and (d) HFD supplemented with n-6 (HFD + n-6). CD + n-6 and HFD + n-6 were supplemented with sunflower oil by oral gavage at 2 g/Kg of body weight, three times per week. CD and HFD were supplemented with water instead at the same dose. HFD induced whole and muscle-specific insulin resistance associated with increased inflammatory markers in insulin-sensitive tissues and macrophage cells. Sunflower oil supplementation was not efficient in preventing or reducing these parameters. In addition, the supplementation increased pro-inflammatory cytokine production by macrophages and tissues. Lipid profile, on the other hand, was improved with the sunflower oil supplementation in animals fed HFD. In conclusion, sunflower oil supplementation improves lipid profile, but it does not prevent or attenuate insulin resistance and inflammation induced by HFD in C57BL/6 mice.
Available from: Ana Flávia Marçal Pessoa
- "Control animals received 0.22 g per kg body weight of water by gavage. As published previously, this mode of administration does not alter nutritional parameters (food ingestion, caloric intake, weight gain) or the general health status of the animals (Rodrigues et al., 2010). "
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ABSTRACT: The effects of oral ingestion of oleic (OLA) and linoleic (LNA) acids on wound healing in rats were investigated. LNA increased the influx of inflammatory cells, the concentration of hydrogen peroxide (H(2)O(2)) and cytokine-induced neutrophil chemoattractant-2αβ (CINC-2αβ), and the activation of the transcription factor activator protein-1 (AP-1) in the wound at 1 hour post wounding. LNA decreased the number of inflammatory cells and IL-1, IL-6, and macrophage inflammatory protein-3 (MIP-3) concentrations, as well as NF-κB activation in the wound at 24 hours post wounding. LNA accelerated wound closure over a period of 7 days. OLA increased TNF-α concentration and NF-κB activation at 1 hour post wounding. A reduction of IL-1, IL-6, and MIP-3α concentrations, as well as NF-κB activation, was observed 24 hours post wounding in the OLA group. These data suggest that OLA and LNA accelerate the inflammatory phase of wound healing, but that they achieve this through different mechanisms.
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