1,721,065 research outputs found
Nutrition et fonction immunitaire (Nutrition and immune function)
No full textUn déficit énergétique majeur ainsi que celui en un ou plusieurs nutriments tels vitamines A, B6, B12, C, E, acide folique, zinc, cuivre, fer, sélénium, acides aminés essentiels et acides gras essentiels, peut altérer la fonction immunitaire et augmenter la sensibilité aux infections. Cela est lié à l'implication des nutriments dans les réponses moléculaires et cellulaires du système immunitaire. La correction de ces déficits restaure la fonction immunitaire et améliore la résistance aux infections. Ainsi, une nutrition appropriée est nécessaire pour maintenir chez l'hôte des défenses immunes dirigées contre les bactéries, les virus, les champignons, les parasites, les cellules tumorales. Bien que, chez le sujet sain, les quantités de certains nutriments requises pour l'amélioration des fonctions immunes soient plus importantes que les apports recommandés, les excès de ces nutriments peuvent également altérer les fonctions immunitaires. Quelques nutriments (par exemple la glutamine et l'arginine) peuvent devenir limitant au cours des états d'agression, et de plus en plus de données viennent appuyer l'idée que leur apport peut aider à la guérison du patient. A deficiency of total energy or of one or more essential nutrients, including vitamins A, B6, B12, C, and E, folic acid, zinc, iron, copper, selenium, essential amino acids and essential fatty acids, will impair immune function and increase susceptibility of the host to infectious pathogens. This is most likely because these nutrients are involved in the molecular and cellular responses to challenge of the immune system. Providing these nutrients to deficient individuals restores immune function and improves resistance to infection. Thus, appropriate nutrition is required in order for the host to maintain adequate immune defences towards bacteria, viruses, fungi, parasites and tumour cel circ;s. Although the intakes of several nutrients which result in greatest enhancement of immune function appear to be greater than recommended intakes, excess intake of certain nutrients also impairs immune responses. Some nutrients (e.g. glutamine, arginine) may become limiting in critical illness and there is mounting evidence that provision of these will aid patient recovery
Omega 3 fatty acids for the treatment of dementia and cognitive impairment
No full textThis is the protocol for a review and there is no abstract. The objectives are as follows:Primary objectiveTo evaluate the effect of omega 3 FA supplementation on cognitive functions in patients with dementia or mild cognitive impairment.Secondary objectivesTo assess the effect of omega 3 FA on global disease severity, neuropsychiatric symptoms, quality of life and performance of activities of daily living (ADLs) and to assess the safety and acceptability of omega 3 FA supplementation in patients with dementia and mild cognitive impairment<br/
Polyunsaturated fatty acids and rheumatoid arthritis
No full textRheumatoid arthritis is characterized by infiltration of T lymphocytes, macrophages and plasma cells into the synovium, and the initiation of a chronic inflammatory state that involves overproduction of proinflammatory cytokines and a dysregulated T-helper-1-type response. Eicosanoids synthesized from arachidonic acid and cytokines cause progressive destruction of cartilage and bone. The n-6 polyunsaturated fatty acid [gamma]-linolenic acid is the precursor of di-homo-[gamma]-linolenic acid. The latter and the n-3 polyunsaturated fatty acid eicosapentaenoic acid, which is found in fish oil, are able to decrease the production of arachidonic acid-derived eicosanoids and to decrease the production of proinflammatory cytokines and reactive oxygen species, and the reactivity of lymphocytes. A number of double-blind, placebo-controlled trials of [gamma]-linolenic acid and fish oil in rheumatoid arthritis have shown significant improvements in a variety of clinical outcomes. These fatty acids should be included as part of the normal therapeutic approach to rheumatoid arthritis. However, it is unclear what the optimal dosage of the fatty acids is, or whether there would be extra benefit from using them in combination
N-3 polyunsaturated fatty acids and allergic disease
No full textPurpose of review: With escalating rates of allergic disease, it is vital to explore novel causal pathways. This review examines the evidence for a potential role of changing dietary intake of [omega]-3 polyunsaturated fatty acids in the development, treatment and prevention of allergic diseases.Recent findings: Although it is difficult to determine the contribution of altered (decreased) dietary intake of [omega]-3 polyunsaturated fatty acids to the recent rise in the incidence of allergic disease, there is growing evidence that these nutrients have antiinflammatory properties and may modulate immune responses. These fatty acids have few side effects, and may be of some benefit in established allergic diseases (such as asthma and atopic dermatitis), although these effects are not strong. Because of this limited efficacy in established disease, the focus has shifted to the potential benefits of these immune modulators in earlier life for disease prevention. Two recent preliminary reports in infants suggest that dietary [omega]-3 polyunsaturated fatty acid supplements in pregnancy or in the early postnatal period could have immunomodulatory properties and associated clinical effects, although more studies are now needed. Novel synthetic polyunsaturated fatty acids with more potent and selective antiinflammatory effects may also provide safe therapeutic and preventive strategies in the future.Summary: Dietary factors are important but still under-explored candidates in the search for environmental strategies to reduce the enormous impact of allergic diseases in modernized societies. There is an ongoing need for further research into the role of [omega]-3 polyunsaturated fatty acids in allergic disease, particularly in early life before atopy is established
In vitro effects of eicosanoids derived from different 20-carbon fatty acids on T helper type 1 and T helper type 2 cytokine production in human whole-blood cultures
No full textBackground: Different series prostaglandins (PGs) and leukotrienes (LTs) are synthesized from different 20 carbon fatty acid precursors. The effects of the different series of PGs and LTs on production of T helper type 1 (Th1) and Th2 cytokines by human cells are not well established.Objective: To characterize the influence of PGs and LTs produced from different fatty acid precursors on the Th1 and Th2 cytokine profile in mitogen-stimulated human whole-blood cultures.Methods: Blood from healthy adult males was diluted and cultured with concanavalin A in the presence or absence of a range of concentrations of various PGs or LTs. Cytokine concentrations in culture supernatants were analysed by enzyme-linked immunosorbent assay (ELISA).Results: PGE1, PGE2 and PGE3 significantly and dose-dependently decreased the concentrations of the Th1 cytokines IL-2 and IFN-? by up to 50% and 70%, respectively. The three PGs exhibited similar potency towards IFN-? production. At the highest concentration used (10-6 m) PGE1, but not PGE2 or PGE3, increased the concentration of the Th2 cytokine IL-4 by about 70%. IL-10 production was not affected by PGs. The ratio of the concentrations of IFN-? to IL-4 was significantly decreased at PGE concentrations of 10-7 and 10-6 M with all three PGEs having similar effects. LTB4, LTC4 and LTC5 did not significantly affect production of the cytokines studied.Conclusion: PGE produced from different fatty acids significantly decrease Th1 cytokine production resulting in a shift in the Th1, Th2 balance in favour of a Th2 response. PGE produced from different fatty acid precursors are equipotent in their effects on human T lymphocytes. Thus, although changes in the pattern of dietary fatty intakes may contribute to the increased prevalence of atopic disease, this would probably not be mediated through substitution of one PGE with another from a different series. It may, however, be mediated through a change in the total amount of PGE produced at the site of antigen presentation
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