Effects of dietary ω3 and ω6 lipids and vitamin E on proliferative response, lymphoid cell subsets, production of cytokines by spleen cells, and splenic protein levels for cytokines and oncogenes in MRL/MpJ-lpr/lpr mice11This research was funded by National Institute of Arthritis and Musculoskeletal and Skin Disorders grant IR15AR/AI43517.
“…Fats are used as fuel by lymphocytes; however, when stressed by mitogens, lymphocytes appear to increase their metabolism with glucose use [21,26]. In addition, the quantity and type of dietary lipids modulates the biochemistry of the cellular immune system, including the production and expression of cytokines [27]. Omega-6 dietary lipids generally increase the levels of pro-inflammatory cytokines and inflammatory PGs, whereas omega-3 lipids may decrease the levels of such cytokines and inflammatory PGs [28].…”
Despite the numerous positive effects of physical exercise, some negative physiological changes occur in long-lasting heavy training with transient dysfunction of the immune system, increased inflammation, and oxidative stress. This is the case of elite athletes, who train intensively to compete at the highest levels. However, these athletes can counteract the negative effects of heavy training, reducing acute and chronic inflammations and supporting the immune system, with nutritional and supplementation countermeasures. For this purpose, macronutrient manipulation with an appropriate use of certain supplements can be considered as an intervention to reduce exercise-induced immune changes and inflammatory risk. For example, branched-chain amino acid (BCAA) supplementation may promote such immune responses in skeletal muscle. Furthermore, micronutrients play an important role in immune function; in particular, the antioxidant capacity of several dietary micronutrients (e.g., tocopherols, docosahexaenoate, and flavonoids) is very interesting to support the endogenous antioxidant defense systems of the athletes, counterbalancing the negative effects of oxidative damage due to free radicals. Some of these nutrients have potential anti-inflammatory properties as assessed by the attenuated levels of interleukin-6 (IL-6) and C-reactive protein (CRP). Key Teaching Points: Long-lasting heavy training plan and competition can lead to chronic immune suppression in athletes, increasing infection risk. Chronic exercise increases mobilization of neutrophils, decreases mobilization of lymphocytes, and decreases the absolute and relative numbers of neutrophils at rest. Nutritional deficiencies alter the immuno-system and increase infection risk. Nutrition can influence exercise-induced immune suppression. Elite athletes competing at the highest levels can benefit from nutritional and supplementation support to improve immunity and reduce acute and chronic inflammations.
“…Fats are used as fuel by lymphocytes; however, when stressed by mitogens, lymphocytes appear to increase their metabolism with glucose use [21,26]. In addition, the quantity and type of dietary lipids modulates the biochemistry of the cellular immune system, including the production and expression of cytokines [27]. Omega-6 dietary lipids generally increase the levels of pro-inflammatory cytokines and inflammatory PGs, whereas omega-3 lipids may decrease the levels of such cytokines and inflammatory PGs [28].…”
Despite the numerous positive effects of physical exercise, some negative physiological changes occur in long-lasting heavy training with transient dysfunction of the immune system, increased inflammation, and oxidative stress. This is the case of elite athletes, who train intensively to compete at the highest levels. However, these athletes can counteract the negative effects of heavy training, reducing acute and chronic inflammations and supporting the immune system, with nutritional and supplementation countermeasures. For this purpose, macronutrient manipulation with an appropriate use of certain supplements can be considered as an intervention to reduce exercise-induced immune changes and inflammatory risk. For example, branched-chain amino acid (BCAA) supplementation may promote such immune responses in skeletal muscle. Furthermore, micronutrients play an important role in immune function; in particular, the antioxidant capacity of several dietary micronutrients (e.g., tocopherols, docosahexaenoate, and flavonoids) is very interesting to support the endogenous antioxidant defense systems of the athletes, counterbalancing the negative effects of oxidative damage due to free radicals. Some of these nutrients have potential anti-inflammatory properties as assessed by the attenuated levels of interleukin-6 (IL-6) and C-reactive protein (CRP). Key Teaching Points: Long-lasting heavy training plan and competition can lead to chronic immune suppression in athletes, increasing infection risk. Chronic exercise increases mobilization of neutrophils, decreases mobilization of lymphocytes, and decreases the absolute and relative numbers of neutrophils at rest. Nutritional deficiencies alter the immuno-system and increase infection risk. Nutrition can influence exercise-induced immune suppression. Elite athletes competing at the highest levels can benefit from nutritional and supplementation support to improve immunity and reduce acute and chronic inflammations.
“…The α-linolenic acid (ALA), linoleic acid (LA), and gamma linolenic acid (GLA) have also shown a signifi cant inhibitory action on TNF-α and on the IL-2 secretion. 20,21,23,37,39,42,43 Some studies have reported that EPA can infl uence physiological processes, protecting against cardiovascular problems and infl ammatory diseases, such as SLE. 44 On the other hand, ω-6 PUFA can exacerbate SLE by inducing the infl ammatory mediators.…”
The authors reviewed the infl uence of nutritional factors on systemic lupus erythematosus (SLE) and discussed an alternative treatment option. The autoimmunity and infl ammatory process of SLE are related to the presence of dyslipidemia, obesity, systemic arterial hypertension, and metabolic syndrome, which should be properly considered to decrease cardiovascular risk. A diet with moderate protein and energy content, but rich in vitamins, minerals (especially antioxidants), and mono/ polyunsaturated fatty acids can promote a benefi cial protective effect against tissue damage and suppression of infl ammatory activity, in addition to helping the treatment of those comorbidities. Diet therapy is a promising approach and some recommendations may offer a better quality of life to patients with SLE.
“…Administration of ascorbic acid (vitamin C) [93] in high doses (0.5-2 g/kg) prior to onset of disease symptoms to rats with adjuvant-induced arthritis has also been reported to dose-dependently reduce paw swelling and infiltration of inflammatory cells into the synovial tissues [94]. Other nutritional antioxidants such as omega-3 fatty acids, [95] and diets rich in fish oil have also shown benefit in animal models of arthritis (for a thorough review see [13]). Rats fed a diet rich in polyphenol-supplemented virgin olive oil prior to induction of antigen-induced arthritis and throughout the course of the study demonstrated reduced paw swelling [96].…”
Section: Antioxidant Therapy In Experimental Arthritismentioning
Oxidant stress as a result of increased production of reactive oxygen species (ROS) or a reduction in the body's endogenous antioxidant defense system is a hallmark of chronic inflammatory diseases including rheumatoid arthritis (RA). A primary source of ROS in RA is leukocytes (i.e. activated macrophages, neutrophils, mast cells and lymphocytes) that are recruited to, and that accumulate within, the synovium. ROS and reactive nitrogen species (RNS) can contribute to the pathogenesis of RA in a variety of ways including: induction of membrane oxidation and instability, irreversible damage to proteins and DNA, cartilage damage and induction of bone resorption. In addition, it has recently been appreciated that ROS/RNS can also modulate a variety of signaling events that control gene expression and effect cellular processes that participate in chronic inflammation. These include effects on vascular tone, cell growth and proliferation and induction of pro-inflammatory genes. Consistent with a role for oxidant stress in the pathogenesis of RA, a number of preclinical and clinical studies have correlated increases in markers of oxidative stress and lower levels of the body's natural antioxidants with disease severity. Accordingly, a variety of methods aimed at reducing ROS production, scavenging ROS or restoring the antioxidant balance have been tested with some success in experimental models of RA and in clinical trials. Although considerable data supports the notion that antioxidant-based drugs could prove beneficial in the treatment of RA, very few have been evaluated clinically and to date none have demonstrated clinical proof-ofconcept in Phase II clinical studies.
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