Volume 89
Progress in Inflammation Research
Series Editors
Michael J. Parnham
Institute of Clinical Pharmacology, Goethe University Frankfurt, Frankfurt am Main, Germany
Thorsten J. Maier
Federal Institute for Vaccines and Biomedicines, Paul Ehrlich Institute, Langen, Germany
Emanuela Ricciotti
Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA
This book series addresses all key topical aspects of basic research, therapy and its clinical implications in the field of inflammatory diseases. It provides a unique reference source for academic and industrial biomedical researchers, drug development personnel, immunologists, rheumatologists, cardiologists, allergologists and many other relevant clinical disciplines. Each publication supplies regular scientific updates on newest developments and allow providing access to state-of-the-art techniques and technologies.
The series gathers knowledge from leading authorities on the multiple facets of inflammation research, making it a valuable asset for advanced students in biomedical sciences, early career investigators and for professionals in both basic and translational research and in the clinic. Each volume comprises a carefully selected collection of high-quality review articles on the respective field of expertise. They also introduce new investigators to the most pertinent aspects of inflammatory disease and allow established investigators to understand fundamental ideas, concepts and data on sub-fields that they may not normally follow.
Thus chapters should not comprise extensive data reviews nor provide a means for authors to present new data that would normally be published in peer-reviewed journals. Instead, the chapters should provide a concise overview and guide to the most pertinent and important literature, thus reflecting a conceptual approach rather than a complete review of the particular field of research. Moreover, each chapter should be intelligible for less experienced researchers or even newcomers to the fields of pathology, mechanisms and therapy of inflammatory disease. To this end, authors should consider introducing PhD students or postdocs who are new to the laboratory to the major concepts and the most critical literature in their chosen field of research.
PIR volumes have been accepted for indexing in Scopus back to publications in 2005.
More information about this series at https://link.springer.com/bookseries/4983
Editors
Graham A. W. Rook and Christopher A. Lowry
Evolution, Biodiversity and a Reassessment of the Hygiene Hypothesis
Logo of the publisher
Editors
Graham A. W. Rook
Centre for Clinical Microbiology, UCL (University College London), London, UK
Christopher A. Lowry
Dept. of Integrative Physiology UCB 603, University of Colorado Boulder, Boulder, CO, USA
ISSN 1422-7746 e-ISSN 2296-4525
Progress in Inflammation Research
ISBN 978-3-030-91050-1 e-ISBN 978-3-030-91051-8
https://doi.org/10.1007/978-3-030-91051-8
The Editor(s) (if applicable) and The Author(s), under exclusive license to Springer Nature Switzerland AG 2022
This work is subject to copyright. All rights are solely and exclusively licensed by the Publisher, whether the whole or part of the material is concerned, specifically the rights of translation, reprinting, reuse of illustrations, recitation, broadcasting, reproduction on microfilms or in any other physical way, and transmission or information storage and retrieval, electronic adaptation, computer software, or by similar or dissimilar methodology now known or hereafter developed.
The use of general descriptive names, registered names, trademarks, service marks, etc. in this publication does not imply, even in the absence of a specific statement, that such names are exempt from the relevant protective laws and regulations and therefore free for general use.
The publisher, the authors and the editors are safe to assume that the advice and information in this book are believed to be true and accurate at the date of publication. Neither the publisher nor the authors or the editors give a warranty, expressed or implied, with respect to the material contained herein or for any errors or omissions that may have been made. The publisher remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.
This Springer imprint is published by the registered company Springer Nature Switzerland AG
The registered company address is: Gewerbestrasse 11, 6330 Cham, Switzerland
Preface
The development and physiological functions of most, probably all, multicellular organisms require interactions with microorganisms. These interactions include signals that modulate organ development and function, data for the immune system, and colonisation; DNA of the microbiota encodes a huge, flexible repertoire of metabolic functions. It is broadly accepted that modern lifestyles have diminished or distorted some of these essential microbial interactions, and that this has contributed to simultaneous increases in a range of localised chronic inflammatory disorders (allergies, autoimmunity, and inflammatory bowel diseases) and also to systemic chronic inflammatory states with persistently raised biomarkers of inflammation, predisposing to metabolic, cardiovascular, and psychiatric problems. This volume explores all of these issues.
The hygiene hypothesis was born in the field of allergic disorders. Awareness of an increase in allergies associated with wealth and urbanisation can be traced back to the nineteenth century when Blackley noted that hay fever was less prevalent amongst the common people than amongst city dwellers [1]. Then in 1989 David Strachan observed that hay fever was less common in children with multiple older siblings, and suggested this could be explained if allergic diseases were prevented by infections in early childhood [2].
This suggestion became known as the hygiene hypothesis, initially focussed on allergic disorders and on the possible role of reduced exposure to the common infections of childhood. But those infections of early childhood (measles, etc.) are mostly Crowd Infections that did not enter human populations until recently; measles, for example, probably transferred to humans during the Roman Empire. Moreover, epidemiological studies have shown that the common infections of childhood make allergies worse, not better.
We cannot be in a state of evolved dependence on the crowd infections of childhood. Nevertheless, those infections, or the vaccines that now prevent them, might play roles in priming immunoregulation. Moreover, some authors believe that we are suffering from the absence of infections such as Helicobacter pylori and helminths that, unlike the crowd infections, were often present in our hunter-gatherer ancestors. These controversial issues are discussed in a broad outline chapter in this volume [3].
So which microorganisms do we need to encounter? We do not have a detailed answer, but we do have two broad principles. First, we know that exposure to the microbiota of mother (and other family members) is crucially important. This probably explains the observations of Strachanthe older siblings enhanced exposure to the family microbiota. Development of the childs microbiota is discussed in detail [4].