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      Nutrition in chronic inflammatory conditions: Bypassing the mucosal block for micronutrients

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          Abstract

          Nutritional Immunity is one of the most ancient innate immune responses, during which the body can restrict nutrients availability to pathogens and restricts their uptake by the gut mucosa (mucosal block). Though this can be a beneficial strategy during infection, it also is associated with non‐communicable diseases—where the pathogen is missing; leading to increased morbidity and mortality as micronutritional uptake and distribution in the body is hindered. Here, we discuss the acute immune response in respect to nutrients, the opposing nutritional demands of regulatory and inflammatory cells and particularly focus on some nutrients linked with inflammation such as iron, vitamins A, Bs, C, and other antioxidants. We propose that while the absorption of certain micronutrients is hindered during inflammation, the dietary lymph path remains available. As such, several clinical trials investigated the role of the lymphatic system during protein absorption, following a ketogenic diet and an increased intake of antioxidants, vitamins, and minerals, in reducing inflammation and ameliorating disease.

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          Reactive oxygen species in inflammation and tissue injury.

          Abstract Reactive oxygen species (ROS) are key signaling molecules that play an important role in the progression of inflammatory disorders. An enhanced ROS generation by polymorphonuclear neutrophils (PMNs) at the site of inflammation causes endothelial dysfunction and tissue injury. The vascular endothelium plays an important role in passage of macromolecules and inflammatory cells from the blood to tissue. Under the inflammatory conditions, oxidative stress produced by PMNs leads to the opening of inter-endothelial junctions and promotes the migration of inflammatory cells across the endothelial barrier. The migrated inflammatory cells not only help in the clearance of pathogens and foreign particles but also lead to tissue injury. The current review compiles the past and current research in the area of inflammation with particular emphasis on oxidative stress-mediated signaling mechanisms that are involved in inflammation and tissue injury.
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            The gut microbiota shapes intestinal immune responses during health and disease.

            Immunological dysregulation is the cause of many non-infectious human diseases such as autoimmunity, allergy and cancer. The gastrointestinal tract is the primary site of interaction between the host immune system and microorganisms, both symbiotic and pathogenic. In this Review we discuss findings indicating that developmental aspects of the adaptive immune system are influenced by bacterial colonization of the gut. We also highlight the molecular pathways that mediate host-symbiont interactions that regulate proper immune function. Finally, we present recent evidence to support that disturbances in the bacterial microbiota result in dysregulation of adaptive immune cells, and this may underlie disorders such as inflammatory bowel disease. This raises the possibility that the mammalian immune system, which seems to be designed to control microorganisms, is in fact controlled by microorganisms.
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              The gut microbiota influences blood-brain barrier permeability in mice.

              Pivotal to brain development and function is an intact blood-brain barrier (BBB), which acts as a gatekeeper to control the passage and exchange of molecules and nutrients between the circulatory system and the brain parenchyma. The BBB also ensures homeostasis of the central nervous system (CNS). We report that germ-free mice, beginning with intrauterine life, displayed increased BBB permeability compared to pathogen-free mice with a normal gut flora. The increased BBB permeability was maintained in germ-free mice after birth and during adulthood and was associated with reduced expression of the tight junction proteins occludin and claudin-5, which are known to regulate barrier function in endothelial tissues. Exposure of germ-free adult mice to a pathogen-free gut microbiota decreased BBB permeability and up-regulated the expression of tight junction proteins. Our results suggest that gut microbiota-BBB communication is initiated during gestation and propagated throughout life.
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                Author and article information

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                Journal
                Allergy
                Allergy
                0105-4538
                1398-9995
                February 2024
                December 12 2023
                February 2024
                : 79
                : 2
                : 353-383
                Affiliations
                [1 ] Comparative Medicine, The Interuniversity Messerli Research Institute of the University of Veterinary Medicine Vienna Medical University Vienna and University Vienna Vienna Austria
                [2 ] Institute of Pathophysiology and Allergy Research, Center of Pathophysiology, Infectiology and Immunology Medical University of Vienna Vienna Austria
                [3 ] Department of Translational Medical Science and ImmunoNutritionLab at CEINGE‐Advanced Biotechnologies University of Naples "Federico II" Naples Italy
                [4 ] Department of Medicine, School of Microbiology, APC Microbiome Ireland University College Cork Cork Ireland
                [5 ] Section of Paediatrics, Department of Clinical and Experimental Medicine University of Pisa Pisa Italy
                [6 ] Swiss Institute of Allergy and Asthma Research (SIAF) University of Zürich Davos Switzerland
                [7 ] Christine Kühne ‐ Center for Allergy Research and Education (CK‐CARE) Davos Switzerland
                [8 ] Pediatric Area, Fondazione IRCCS Ca' Granda‐Ospedale Maggiore Policlinico Milan Italy
                [9 ] Department of Nutritional Sciences and Dietetics International Hellenic University Thessaloniki Greece
                [10 ] Children's Hospital Colorado University of Colorado Aurora Colorado USA
                Article
                10.1111/all.15972
                38084827
                88ea2a97-53b9-4a1e-aa39-86ca57666bc9
                © 2024

                http://creativecommons.org/licenses/by-nc/4.0/

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