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    Immune cells and microbiota response to iron starvation

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    Metal ions are essential for life on Earth, mostly as crucial components of all living organisms; indeed, they are necessary for bioenergetics functions as crucial redox catalysts. Due to the essential role of iron in biological processes, body iron content is finely regulated and is the battlefield of a tug-of-war between the host and the microbiota.Iron availability in the intestinal lumen could prevent or promote intestinal dysbiosis, although current data do not provide a definitive response. Recent data demonstrated that nutritional derived polyphenols explicit their anti-inflammatory functions sequestrating iron from immune cells. Here, we discuss whether nutritional iron chelators could be able to change the gut microbiota composition and prevent the intestinal dysbiosis associated with intestinal chronic inflammatory syndromes.Iron is lost by cellular exfoliation and occasional bleeding; it is absorbed from nutritional components. Heme is the most important source of dietary iron, while non-heme iron can be absorbed only in the duodenum and the beginning of the jejunum in pH permissive (acid) conditions. Western diets often contain large quantities of foods characterized by a high heme-iron content like meat, fish, and poultry, and small quantities of non-heme-iron content like vegetables, fruits, and nuts. Furthermore, nutritional substances can affect iron absorption: ascorbic acid is an efficient enhancer of non-heme-iron absorption, vice versa, phytic acid is known to be among the major iron absorption inhibitors, and iron-chelating substances like quercetin inhibit its absorption, likely due to loss of chelated-iron solubility.Iron deficiency is the most common cause of anemia worldwide and one of the most common complications observed in inflammatory bowel disease (IBD) patients due to gastrointestinal hemorrhages. In IBD patients, the guidelines for the management of iron deficiency are not entirely satisfactory because following oral iron supplementation patients sometimes report worsening of the IBD symptoms (1). Interestingly, iron supplemented diets can also show protective effects in dextran sodium sulfate (DSS)-induced colitis models. Constante et al. demonstrated that iron formulation dramatically changed the outcome of the DSS-induced colitis, as oral supplementation with ferrous bisglycinate but not ferric ethylenediaminetetraacetic acid enhanced the beneficial action of probiotics (2)

    Looking at flavonoid biodiversity in horticultural crops: A colored mine with nutritional benefits

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    Flavonoids represent a wide group of plant secondary metabolites implicated in many physiological roles, from the attraction of pollinators to the protection against biotic or abiotic stresses. Flavonoids are synthetized in a number of horticultural crops that are important components of our daily diet. In the last decades, the consumption of vegetables rich in antioxidants has been strongly promoted from the perspective of prevention/protection against chronic diseases. Therefore, due to their nutritional importance, several attempts have been made to enhance flavonoid levels in species of agronomic interest. In this review, we focus on the flavonoid biodiversity among the major horticultural species, which is responsible of differences among closely related species and influences the qualitative/quantitative composition. We also review the role of flavonoids in the nutritional quality of plant products, contributing to their organoleptic and nutritional properties, and the main strategies of biofortification to increase their content

    Interactions among dendritic cells, macrophages, and epithelial cells in the gut: implications for immune tolerance

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    The intestine is described as an immune privileged site where immunoregulatory mechanisms simultaneously defend against pathogens, yet preserve tissue homeostasis to avoid immune-mediated pathology in response to environmental challenges. Additionally, tolerance to ingested antigens promotes the development of systemic unresponsiveness towards the same antigens. It is increasingly clear that this tolerance is a complex process that derives from the coordinated action of both canonical immune and non-immune cells at mucosal sites, including dendritic cells, macrophages and epithelial cells. Recent evidence suggests that dysregulation in gut-induced tolerance and commensal bacterial handling affects both local and systemic compartments and contributes to autoimmune disease. Understanding how tolerance is achieved at mucosal sites may thus be exploited to re-establish tissue homeostasis. © 2008 Elsevier Ltd. All rights reserved
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