The Human Microbiota and Chronic Disease E-Book

• Herausgeber: John Wiley & Sons
• Kategorie: Wissenschaft und neue Technologien
• Sprache: Englisch

Seitenzahl: 1273

Veröffentlichungsjahr: 2016

Beschreibung

Microbiota-associated pathology can be a direct result of changes in general bacterial composition, such as might be found in periodontitis and bacterial vaginosis, and/or as the result of colonization and/or overgrowth of so called keystone species. The disruption in the composition of the normal human microbiota, or dysbiosis, plays an integral role in human health and human disease.

The Human Microbiota and Human Chronic Disease: Dysbioses as a Cause of Human Pathology discusses the role of the microbiota in maintaining human health. The text introduces the reader to the biology of microbial dysbiosis and its potential role in both bacterial disease and in idiopathic chronic disease states.

Divided into five sections, the text delineates the concept of the human bacterial microbiota with particular attention being paid to the microbiotae of the gut, oral cavity and skin. A key methodology for exploring the microbiota, metagenomics, is also described. The book then shows the reader the cellular, molecular and genetic complexities of the bacterial microbiota, its myriad connections with the host and how these can maintain tissue homeostasis. Chapters then consider the role of dysbioses in human disease states, dealing with two of the commonest bacterial diseases of humanity – periodontitis and bacterial vaginosis. The composition of some, if not all microbiotas can be controlled by the diet and this is also dealt with in this section.  The discussion moves on to the major ‘idiopathic’ diseases afflicting humans, and the potential role that dysbiosis could play in their induction and chronicity. The book then concludes with the therapeutic potential of manipulating the microbiota, introducing the concepts of probiotics, prebiotics and the administration of healthy human faeces (faecal microbiota transplantation), and then hypothesizes as to the future of medical treatment viewed from a microbiota-centric position.

• Provides an introduction to dysbiosis, or a disruption in the composition of the normal human microbiota
• Explains how microbiota-associated pathology and other chronic diseases can result from changes in general bacterial composition
• Explores the relationship humans have with their microbiota, and its significance in human health and disease
• Covers host genetic variants and their role in the composition of human microbial biofilms, integral to the relationship between human health and human disease

Authored and edited by leaders in the field, The Human Microbiota and Human Chronic Disease will be an invaluable resource for clinicians, pathologists, immunologists, cell and molecular biologists, biochemists, and system biologists studying cellular and molecular bases of human diseases.

Leseprobe

The Human Microbiota and Chronic Disease

Dysbiosis as a Cause of Human Pathology

EDITED BY

Luigi Nibali

Queen Mary University of London, London, United Kingdom

Brian Henderson

University College London, London, United Kingdom

Copyright © 2016 by John Wiley & Sons, Inc. All rights reserved

Published by John Wiley & Sons, Inc., Hoboken, New JerseyPublished simultaneously in Canada

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Library of Congress Cataloging-in-Publication Data

Names: Henderson, Brian (Professor), editor. | Nibali, Luigi, 1978– editor.Title: The human microbiota and chronic disease : dysbiosis as a cause of human pathology / edited by Luigi Nibali and Brian Henderson.Description: Hoboken, New Jersey : John Wiley & Sons, 2016. | Includes bibliographical references and index.Identifiers: LCCN 2016016110 (print) | LCCN 2016025000 (ebook) | ISBN 9781118982877 (cloth) | ISBN 9781118982884 (pdf) | ISBN 9781118982891 (epub)Subjects: LCSH: Human body–Microbiology. | Chronic diseases.Classification: LCC QR46 .H83 2016 (print) | LCC QR46 (ebook) | DDC 616.9/041–dc23LC record available at https://lccn.loc.gov/2016016110

Cover credit: Gettyimages/STEVE GSCHMEISSNER/SPL

List of contributors

Luis G. Bermúdez-HumaránAgroParisTech; UMR1319 Micalis; F-78350 Jouy-en-Josas, France; INRA, UMR1319 Micalis, Commensal and Probiotics-Host Interactions Laboratory, Domaine de Vilvert, 78352 Jouy-en-Josas Cedex, France

Aadil BharwaniThe Brain-body Institute and Firestone Institute for Respiratory Health, Ontario, Canada

Hervé M. BlottièreMicalis Institute, INRA, AgroParisTech, Universitè Paris-Saclay, Paris, France

Katharina BrandlSkaggs School of Pharmacy, University of California, San Diego, United States

Holger BrüggemannDepartment of Biomedicine, Aarhus University, Aarhus, Denmark

Eugenia BruzzeseUniversity of Naples, Naples, Italy

Vittoria BuccigrossiUniversity of Naples, Naples, Italy

Marie-José ButelUniversité Paris Descartes, Sorbonne Paris, Paris, France

John D. CarterUniversity of South Florida Morsani College of Medicine, Tampa, FL, United States

Séverine CouffinUPEC, Université Paris Est Créteil Val de Marne-Equipe Universitaire EC2M3, Paris, France

Mike CurtisInstitute of Dentistry, Queen Mary University of London

Jacqueline DetertCharité-Universitätsmedizin Berlin, Berlin, Germany

Nik DingSt. Mark’s Hospital, London, United Kingdom

Joël DoréMicalis Institute, INRA, AgroParisTech, Universitè Paris-Saclay, Paris, France

Alan EbringerKing’s College London, London, United Kingdom

Mehrbod EstakiThe University of British Columbia, Kelowna, Canada

Frida FåkLund University, Lund, Sweden

Paul ForsytheMcMaster University, Hamilton, Ontario, Canada

Ralph FrancesconeFox Chase Cancer Center, Cancer Prevention and Control, Philadelphia, United States

Lionel FryImperial College, London, United Kingdom

Markus B. GeukingMucosal Immunology Lab, University of Bern, Switzerland

Deanna L. GibsonThe University of British Columbia, Kelowna, Canada

Alfredo GuarinoUniversity of Naples,Naples, Italy

George HajishengallisSchool of Dental Medicine, University of Pennsylvania, Philadelphia, United States

Ailsa HartSt. Mark’s Hospital, London, United Kingdom

Phillip HaySt. George’s, University of London, United Kingdom

Almut HeinkenLuxembourg Centre for Systems Biomedicine, University of Luxembourg, Belval, Luxembourg

Brian HendersonUniversity College London, London, United Kingdom

Anne-Judith Waligora-DuprietUniversité Paris Descartes, Sorbonne paris, Paris, France

Richard J. LamontSchool of Dentistry, University of Louisville, Louisville, KY, United States

Benjamin J. MarslandService de Pneumologie, CHUV, Faculty of Biology and Medicine, University of Lausanne, Lausanne, Switzerland

Luigi NibaliCentre for Oral Clinical Research, Queen Mary University of London, London, United Kingdom

Candice QuinThe University of British Columbia, Kelowna, Canada

Taha RashidKing’s College London, London, United Kingdom

Giusy RanucciUniversity of Naples, Naples, Italy

Dmitry A. RavcheevLuxembourg Centre for Systems Biomedicine, University of Luxembourg, Belval, Luxembourg

Frank RyanThe Academic Unit of Medical Education, University of Sheffield, United Kingdom

Olawale SalamiService de Pneumologie, CHUV, Faculty of Biology and Medicine, University of Lausanne, Lausanne, Switzerland

S. Tariq SadiqSt. George’s, University of London, United Kingdom

Joost SchalkwijkDepartment of Dermatology, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands

Bernd SchnablUniversity of California, San Diego, United States

Boris A. ShenderovLaboratory of Biology of Bifidobacteria, Head of Research Group Probiotics and Functional Foods, Gabrichevsky Research Institute of Epidemiology and Microbiology, Moscow, Russia

Jessica SnowdenUniversity of Nebraska Medical Center, Omaha, Nebraska United States

Iradj SobhaniCentre Hospitalier Universitaire Henri Mondor-Assistance Publique Hôpitaux, de Paris, Paris, France

Ines ThieleLuxembourg Centre for Systems Biomedicine, University of Luxembourg, Belval, Luxembourg

Andrea Lo VecchioUniversity of Naples, Naples, Italy

Débora B. Vendramini-CostaInstitute of Chemistry, University of Campinas, Campinas-SP, Brazil

William G. WadeCentre for Immunobiology, Blizard Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London, United Kingdom

Clyde WilsonKing Edward VII Memorial Hospital, Bermuda

Michael WilsonUCL Eastman Dental Institute, University College London, United Kingdom

Kazuhisa YamazakiDivision of Oral Science for Health Promotion, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan

Patrick L.J.M. ZeeuwenDepartment of Dermatology, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands

Preface

The human organism comprises 1013 eukaryotic cells divided into a large number of distinct organs and tissues, with unimaginable requirements for inter- and intra-cellular communication. Malfunction in such communication inevitably results in the state we define as human disease. The emergent properties of the eukaryotic cellular complexity in Homo sapiens were beginning to be suspected in the 1950s and 1960s, when it was becoming clear that the bacteria that actually existed within the healthy human could have a major influence on many of its cellular and tissue systems, including innate and adaptive immunity. The development of antibiotic resistance in the 1970s produced a renaissance in microbiology that revealed just how heavily colonised healthy vertebrates were with bacteria. The human appears to be the acme of this colonisation process and it is now a familiar expression that ‘for every human cell in our bodies there are ten bacteria’. Not only are we colonised by around 1014 bacteria, but the human population carries round with it a diversity of bacterial phylotypes that swamps the diversity of all the species in the aggregate of the world’s zoological collections. Thus we can no longer think of bacteria in terms of ‘us’ and ‘them’. Homo sapiens, like most vertebrates, must be viewed as a supra-organism colonised, on its mucosal surfaces and on the skin (and who knows where else) with complex populations of bacteria; each individual has a unique mixture of these bacteria, presumably a result of genetic (and/or epigenetic) factors controlling commensal bacterial colonisation and the stability of such colonisation.