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      Immune Vulnerability of Infants to Tuberculosis

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          Abstract

          One of the challenges faced by the infant immune system is learning to distinguish the myriad of foreign but nonthreatening antigens encountered from those expressed by true pathogens. This balance is reflected in the diminished production of proinflammatory cytokines by both innate and adaptive immune cells in the infant. A downside of this bias is that several factors critical for controlling Mycobacterium tuberculosis infection are significantly restricted in infants, including TNF, IL-1, and IL-12. Furthermore, infant T cells are inherently less capable of differentiating into IFN- γ -producing T cells. As a result, infected infants are 5–10 times more likely than adults to develop active tuberculosis (TB) and have higher rates of severe disseminated disease, including miliary TB and meningitis. Infant TB is a fundamentally different disease than TB in immune competent adults. Immunotherapeutics, therefore, should be specifically evaluated in infants before they are routinely employed to treat TB in this age group. Modalities aimed at reducing inflammation, which may be beneficial for adjunctive therapy of some forms of TB in older children and adults, may be of no benefit or even harmful in infants who manifest much less inflammatory disease.

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          Functional interactions between the gut microbiota and host metabolism.

          The link between the microbes in the human gut and the development of obesity, cardiovascular disease and metabolic syndromes, such as type 2 diabetes, is becoming clearer. However, because of the complexity of the microbial community, the functional connections are less well understood. Studies in both mice and humans are helping to show what effect the gut microbiota has on host metabolism by improving energy yield from food and modulating dietary or the host-derived compounds that alter host metabolic pathways. Through increased knowledge of the mechanisms involved in the interactions between the microbiota and its host, we will be in a better position to develop treatments for metabolic disease.
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            Host-gut microbiota metabolic interactions.

            The composition and activity of the gut microbiota codevelop with the host from birth and is subject to a complex interplay that depends on the host genome, nutrition, and life-style. The gut microbiota is involved in the regulation of multiple host metabolic pathways, giving rise to interactive host-microbiota metabolic, signaling, and immune-inflammatory axes that physiologically connect the gut, liver, muscle, and brain. A deeper understanding of these axes is a prerequisite for optimizing therapeutic strategies to manipulate the gut microbiota to combat disease and improve health.
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              Toll-like receptor triggering of a vitamin D-mediated human antimicrobial response.

               P Liu (2006)
              In innate immune responses, activation of Toll-like receptors (TLRs) triggers direct antimicrobial activity against intracellular bacteria, which in murine, but not human, monocytes and macrophages is mediated principally by nitric oxide. We report here that TLR activation of human macrophages up-regulated expression of the vitamin D receptor and the vitamin D-1-hydroxylase genes, leading to induction of the antimicrobial peptide cathelicidin and killing of intracellular Mycobacterium tuberculosis. We also observed that sera from African-American individuals, known to have increased susceptibility to tuberculosis, had low 25-hydroxyvitamin D and were inefficient in supporting cathelicidin messenger RNA induction. These data support a link between TLRs and vitamin D-mediated innate immunity and suggest that differences in ability of human populations to produce vitamin D may contribute to susceptibility to microbial infection.
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                Author and article information

                Journal
                Clin Dev Immunol
                Clin. Dev. Immunol
                CDI
                Clinical and Developmental Immunology
                Hindawi Publishing Corporation
                1740-2522
                1740-2530
                2013
                13 May 2013
                : 2013
                Affiliations
                1Centre for Understanding and Preventing Infections in Children, Child & Family Research Institute, University of British Columbia, Vancouver, BC, Canada V5Z 4H4
                2Department of Pediatrics, Laboratory of Pediatric Infectious Diseases, Radboud University Medical Centre, 6500 HB Nijmegen, The Netherlands
                3Sydney Institute for Emerging Infectious Diseases and Biosecurity and The Children's Hospital at Westmead, University of Sydney, Locked Bag 4100, Sydney, NSW 2145, Australia
                4Department of Immunology, University of Washington, Seattle, WA 98195, USA
                5Seattle Biomedical Research Institute, Seattle, WA 98109, USA
                6Department of Pediatrics, University of Washington, Seattle, WA 98195, USA
                Author notes
                *Koen Vanden Driessche: koen.vandendriessche@ 123456cw.bc.ca and

                Academic Editor: Tobias R. Kollmann

                Article
                10.1155/2013/781320
                3666431
                23762096
                Copyright © 2013 Koen Vanden Driessche et al.

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                Categories
                Review Article

                Immunology

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