9 research outputs found

    Shaping the Gut Microbiota by Breastfeeding: The Gateway to Allergy Prevention?

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    Evidence is accumulating that demonstrates the importance of the gut microbiota in health and diseases such as allergy. Recent studies emphasize the importance of the “window of opportunity” in early life, during which interventions altering the gut microbiota induce long-term effects. The neonate's gut microbiota composition and metabolism could therefore play an essential role in allergic disease risk. Breastfeeding shapes the gut microbiota in early life, both directly by exposure of the neonate to the milk microbiota and indirectly, via maternal milk factors that affect bacterial growth and metabolism such as human milk oligosaccharides, secretory IgA, and anti-microbial factors. The potential of breastmilk to modulate the offspring's early gut microbiota is a promising tool for allergy prevention. Here, we will review the existing evidence demonstrating the impact of breastfeeding on shaping the neonate's gut microbiota and highlight the potential of this strategy for allergy prevention

    Shaping the Gut Microbiota by Breastfeeding : The Gateway to Allergy Prevention?

    No full text
    Evidence is accumulating that demonstrates the importance of the gut microbiota in health and diseases such as allergy. Recent studies emphasize the importance of the "window of opportunity" in early life, during which interventions altering the gut microbiota induce long-term effects. The neonate's gut microbiota composition and metabolism could therefore play an essential role in allergic disease risk. Breastfeeding shapes the gut microbiota in early life, both directly by exposure of the neonate to the milk microbiota and indirectly, via maternal milk factors that affect bacterial growth and metabolism such as human milk oligosaccharides, secretory IgA, and anti-microbial factors. The potential of breastmilk to modulate the offspring's early gut microbiota is a promising tool for allergy prevention. Here, we will review the existing evidence demonstrating the impact of breastfeeding on shaping the neonate's gut microbiota and highlight the potential of this strategy for allergy prevention

    Shaping the Gut Microbiota by Breastfeeding: The Gateway to Allergy Prevention?

    No full text
    Evidence is accumulating that demonstrates the importance of the gut microbiota in health and diseases such as allergy. Recent studies emphasize the importance of the "window of opportunity" in early life, during which interventions altering the gut microbiota induce long-term effects. The neonate's gut microbiota composition and metabolism could therefore play an essential role in allergic disease risk. Breastfeeding shapes the gut microbiota in early life, both directly by exposure of the neonate to the milk microbiota and indirectly, via maternal milk factors that affect bacterial growth and metabolism such as human milk oligosaccharides, secretory IgA, and anti-microbial factors. The potential of breastmilk to modulate the offspring's early gut microbiota is a promising tool for allergy prevention. Here, we will review the existing evidence demonstrating the impact of breastfeeding on shaping the neonate's gut microbiota and highlight the potential of this strategy for allergy prevention

    Increased intake of vegetable oil rich in n-6 PUFA enhances allergic symptoms and prevents oral tolerance induction in whey-allergic mice

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    Increased intake of vegetable oils rich in n-6 PUFA, including soyabean oil, has been associated with an increase in allergic disease. The present study aimed to determine the effect of an increasing dose of dietary vegetable oil on allergic outcomes in mice. To study this, mice received a 7 v. 10 % soyabean oil diet before and during oral sensitisation with whey or whey hyperimmune serum transfer. Another group of mice received partial whey hydrolysate (pWH) while being fed the diets before oral sensitisation. The acute allergic skin response, serum Ig level, mouse mast cell protease-1 (mMCP-1) concentration and/or splenic T-cell percentages were determined upon whey challenge. When the diets were provided before and during oral sensitisation, the acute allergic skin response was increased in mice fed the 10 % soyabean oil diet compared with the 7 % soyabean oil diet. Whey IgE and IgG1 levels remained unaltered, whereas mMCP-1 levels increased in mice fed the 10 % soyabean oil diet. Furthermore, allergic symptoms were increased in naive mice fed the 10 % soyabean oil diet and sensitised with whey hyperimmune serum. In addition to enhancing the mast cell response, the 10 % soyabean oil diet increased the percentage of activated Th1 and Th2 cells as well as increased the ratios of Th2:regulatory T cells and Th2:Th1 when compared with the 7 % soyabean oil diet. Oral tolerance induction by pWH was abrogated in mice fed the 10 % soyabean oil diet compared with those fed the 7 % soyabean oil diet during pretreatment with pWH. In conclusion, increased intake of soyabean oil rich in n-6 PUFA suppresses tolerance induction by pWH and enhances the severity of the allergic effector response in whey-allergic mice. Dietary vegetable oils rich in n-6 PUFA may enhance the susceptibility to develop or sustain food allergy

    Dietary fish oil improves endothelial function and lowers blood pressure via suppression of sphingolipid-mediated contractions in spontaneously hypertensive rats

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    Long-chain n-3 polyunsaturated fatty acids from oily fish reduce blood pressure (BP) in hypertension. Previously, we demonstrated that hypertension is associated with marked alterations in sphingolipid biology and elevated ceramide-induced vasoconstriction. Here we investigated in spontaneously hypertensive rats (SHRs) whether fish oil improves endothelial function including reduced vascular contraction induced via the sphingolipid cascade, resulting in reduced BP. Twelve-week-old SHRs were fed a control or fish oil-enriched diet during 12 weeks, and BP was recorded. Plasma sphingolipid levels were quantified by mass spectrometry and the response of isolated carotid arteries towards different stimuli was measured. Furthermore, erythrocyte membrane fatty acid composition, thromboxane A2 formation and cytokine secretion in ex-vivo lipopolysaccharide-stimulated thoracic aorta segments were determined. The fish oil diet reduced the mean arterial BP (P  < 0.001) and improved endothelial function, as indicated by a substantially increased relaxation potential towards ex-vivo methacholine exposure of the carotid arteries (P  < 0.001). The long-chain n-3 polyunsaturated fatty acid diet resulted in altered levels of specific (glucosyl)ceramide subspecies (P  < 0.05), reduced membrane arachidonic acid content (P  < 0.001) and decreased thromboxane concentrations in plasma (P  < 0.01). Concomitantly, the fish oil diet largely reduced ceramide-induced contractions (P  < 0.01), which are predominantly mediated by thromboxane. Furthermore, thromboxane A2 and interleukin-10 were reduced in supernatants of lipopolysaccharide-stimulated thoracic aorta of SHRs fed the fish oil diet while RANTES (regulated on activation, normal T-cell expressed and secreted) was enhanced. This may contribute to reduced vasoconstriction in vivo. Dietary fish oil lowers BP in SHRs and improves endothelial function in association with suppression of sphingolipid-dependent vascular contractio

    Dietary long chain n-3 polyunsaturated fatty acids prevent impaired social behaviour and normalize brain dopamine levels in food allergic mice

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    Allergy is suggested to exacerbate impaired behaviour in children with neurodevelopmental disorders. We have previously shown that food allergy impaired social behaviour in mice. Dietary fatty acid composition may affect both the immune and nervous system. The aim of this study was to assess the effect of n-3 long chain polyunsaturated fatty acids (n-3 LCPUFA) on food allergy-induced impaired social behaviour and associated deficits in prefrontal dopamine (DA) in mice. Mice were fed either control or n-3 LCPUFA-enriched diet before and during sensitization with whey. Social behaviour, acute allergic skin response and serum immunoglobulins were assessed. Monoamine levels were measured in brain and intestine and fatty acid content in brain. N-3 LCPUFA prevented impaired social behaviour of allergic mice. Moreover, n-3 LCPUFA supplementation increased docosahexaenoic acid (DHA) incorporation into the brain and restored reduced levels of prefrontal DA and its metabolites 3,4-dihydroxyphenylacetic acid, 3-methoxytyramine and homovanillic acid in allergic mice. In addition to these brain effects, n-3 LCPUFA supplementation reduced the allergic skin response and restored decreased intestinal levels of serotonin metabolite 5-hydroxyindoleacetic acid in allergic mice. N-3 LCPUFA may have beneficial effects on food allergy-induced deficits in social behaviour, either indirectly by reducing the allergic response and restoring intestinal 5-HT signalling, or directly by DHA incorporation into neuronal membranes, affecting the DA system. Therefore, it is of interest to further investigate the relevance of food allergy-enhanced impairments in social behaviour in humans and the potential benefits of dietary n-3 LCPUFA supplementation

    Dietary long chain n-3 polyunsaturated fatty acids prevent impaired social behaviour and normalize brain dopamine levels in food allergic mice

    No full text
    Allergy is suggested to exacerbate impaired behaviour in children with neurodevelopmental disorders. We have previously shown that food allergy impaired social behaviour in mice. Dietary fatty acid composition may affect both the immune and nervous system. The aim of this study was to assess the effect of n-3 long chain polyunsaturated fatty acids (n-3 LCPUFA) on food allergy-induced impaired social behaviour and associated deficits in prefrontal dopamine (DA) in mice. Mice were fed either control or n-3 LCPUFA-enriched diet before and during sensitization with whey. Social behaviour, acute allergic skin response and serum immunoglobulins were assessed. Monoamine levels were measured in brain and intestine and fatty acid content in brain. N-3 LCPUFA prevented impaired social behaviour of allergic mice. Moreover, n-3 LCPUFA supplementation increased docosahexaenoic acid (DHA) incorporation into the brain and restored reduced levels of prefrontal DA and its metabolites 3,4-dihydroxyphenylacetic acid, 3-methoxytyramine and homovanillic acid in allergic mice. In addition to these brain effects, n-3 LCPUFA supplementation reduced the allergic skin response and restored decreased intestinal levels of serotonin metabolite 5-hydroxyindoleacetic acid in allergic mice. N-3 LCPUFA may have beneficial effects on food allergy-induced deficits in social behaviour, either indirectly by reducing the allergic response and restoring intestinal 5-HT signalling, or directly by DHA incorporation into neuronal membranes, affecting the DA system. Therefore, it is of interest to further investigate the relevance of food allergy-enhanced impairments in social behaviour in humans and the potential benefits of dietary n-3 LCPUFA supplementation
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