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(BQ) Part 1 book “Inflammation fundamental mechanisms” has contents: TNF superfamily in inflammation, complement as a mediator of inflammation, lipids and inflammation, reactive oxygen species.
10028_9789813109438_tp.indd 28/2/18 12:02 PM 10028_9789813109438_tp.indd 28/2/18 12:02 PM b2530 International Strategic Relations and China’s National Security: World at the Crossroads This page intentionally left blank b2530_FM.indd 01-Sep-16 11:03:06 AM 10028_9789813109438_tp.indd 28/2/18 12:02 PM Published by World Scientific Publishing Co Pte Ltd Toh Tuck Link, Singapore 596224 USA office: 27 Warren Street, Suite 401-402, Hackensack, NJ 07601 UK office: 57 Shelton Street, Covent Garden, London WC2H 9HE Library of Congress Cataloging-in-Publication Data Names: Ley, Klaus, 1957– editor Title: Inflammation : fundamental mechanisms / edited by Klaus Ley Other titles: Inflammation (Ley) Description: New Jersey : World Scientific, 2018 | Includes bibliographical references and index Identifiers: LCCN 2017058719 | ISBN 9789813109438 (hardcover : alk paper) Subjects: | MESH: Inflammation physiopathology Classification: LCC RB131 | NLM QZ 150 | DDC 616/.0473 dc23 LC record available at https://lccn.loc.gov/2017058719 British Library Cataloguing-in-Publication Data A catalogue record for this book is available from the British Library Copyright © 2018 by World Scientific Publishing Co Pte Ltd All rights reserved This book, or parts thereof, may not be reproduced in any form or by any means, electronic or mechanical, including photocopying, recording or any information storage and retrieval system now known or to be invented, without written permission from the publisher For photocopying of material in this volume, please pay a copying fee through the Copyright Clearance Center, Inc., 222 Rosewood Drive, Danvers, MA 01923, USA In this case permission to photocopy is not required from the publisher For any available supplementary material, please visit http://www.worldscientific.com/worldscibooks/10.1142/10028#t=suppl Typeset by Stallion Press Email: enquiries@stallionpress.com Printed in Singapore XiaoLing - 10028 - Inflammation.indd 19-12-17 1:53:46 PM 9x6 b3151 Inflammation: Fundamental Mechanisms Contents Chapter 1 TNF Superfamily in Inflammation arisol Veny, Richard Virgen-Slane M and Carl F Ware Introduction 1.1 Discovery of TNF and lymphotoxin 1.2 Description of TNFSF proteins 1.2.1 TNFSF ligands 1.2.2 TNF receptors superfamily 1.2.3 Ligand-receptor binding models 1.2.4 The lymphotoxin and tumor necrosis factor network 1.3 Signaling pathways 1.3.1 The TNF-TNFR pathway 1.3.2 LTbR signaling and the alternative NF-kB pathway10 TNFSF and inflammation 11 2.1 Acute inflammation 11 2.2 Chronic inflammation and autoimmunity 15 2.3 TNFSF signatures in human pathologies 18 v b3151_FM.indd 06-Mar-18 10:00:07 AM b3151 Inflammation: Fundamental Mechanisms 9x6 vi Inflammation: Fundamental Mechanisms 2.3.1 Rheumatoid arthritis 18 2.3.2 Inflammatory bowel disease 19 2.4 Experimental models and the TNFSF as drug targets 21 Targeting TNFSF in the clinic 26 3.1 TNF inhibitors 26 3.2 Other TNFSF targets 29 Summary 31 Acknowledgements32 References32 Chapter 2 Complement as a Mediator of Inflammation 51 B Paul Morgan b3151_FM.indd Introduction to the complement system 1.1 What is complement? 1.2 Initiation of complement activation 1.3 Amplification in the activation pathways 1.4 The amplification loop of the alternative pathway 1.5 Amplification at the stage of C5 cleavage 1.6 Assembly of the membrane attack complex 1.7 Active products of complement activation 1.8 Complement regulation 1.9 Complement receptors Complement roles in health 2.1 Protection against infection 2.2 Immune complex solubilisation 2.3 Priming adaptive immunity 2.4 Regulating lipid metabolism Complement roles in disease 3.1 Complement and autoimmunity 3.2 Complement deficiencies 3.3 Complement mutations and polymorphisms 51 51 52 52 54 54 55 55 57 57 58 58 58 59 59 60 60 61 63 06-Mar-18 10:00:07 AM 9x6 b3151 Inflammation: Fundamental Mechanisms Contents vii Complement as a driver of inflammation 64 4.1 General principles 64 4.2 Complement anaphylatoxins 65 4.3 Membrane attack complex 68 4.4 Complement and inflammasome activation 70 Complement inhibitors as anti-inflammatory drugs 71 5.1 Pathway blockers as anti-inflammatory drugs 71 5.2 Blocking C3a and C5a to inhibit inflammation 72 Summary and future prospects 73 References74 Chapter 3 Lipids and Inflammation 79 alerie B O’Donnell, Robert C Murphy V and Garret A FitzGerald Introduction Lipids and inflammation in obesity Circulating plasma lipids and inflammation Specific lipid classes in inflammation 4.1 Eicosanoids and related lipids 4.1.1 COX enzymes, products, and their receptors 4.1.2 Inhibition of COXs 4.1.3 COX metabolites in inflammation 4.1.4 LOX enzymes, products, and their receptors 4.1.5 LOX metabolites in inflammation 4.1.6 Transcellular generation of eicosanoids 4.1.7 Endocannabinoids and inflammation 4.1.8 Isoprostanes and inflammation 4.2 Phospholipids in inflammation 4.2.1 Aminophospholipid translocation in inflammation 4.2.2 Oxidized phospholipids in inflammation b3151_FM.indd 79 80 82 84 84 84 87 87 89 91 92 94 96 96 97 97 06-Mar-18 10:00:07 AM b3151 Inflammation: Fundamental Mechanisms 9x6 viii Inflammation: Fundamental Mechanisms 4.2.3 Lysophospholipids (LP) and phosphatidic acid (PA) 100 4.2.4 Phosphoinositides 101 4.3 Ceramides/sphingolipids 103 Lipid receptors in inflammation: PPAR and LXR 105 5.1 Peroxisome proliferator-activated receptors (PPAR) 105 5.2 Liver X receptor (LXR) 107 Lipidomics of inflammation: Analysis of bioactive lipids 107 Summary 109 References109 Chapter 4 Reactive Oxygen Species 125 Ulla G Knaus Introduction 125 Reactive oxygen species 126 2.1 Superoxide 127 2.2 Hydrogen peroxide 128 2.3 Hydroxyl radical 129 2.4 Hypochlorous acid 129 2.5 Oxidative protein modification 130 Oxidant–antioxidant balance 131 ROS sources 135 4.1 H2O2 as secondary enzymatic product 135 4.2 Prokaryotic H2O2 136 • – 4.3 O2 as secondary enzymatic product — Mitochondrial electron transport chain 137 • – 4.4 O2 and H2O2 as primary enzymatic product — NADPH oxidases 139 4.4.1 NOX/DUOX structural organization 140 4.4.2 NOX2 assembly and activation 143 4.4.3 Regulation of other NOX/DUOX family members146 4.4.4 ROS deficiency due to NADPH oxidase variants including CGD 147 b3151_FM.indd 06-Mar-18 10:00:07 AM 9x6 b3151 Inflammation: Fundamental Mechanisms Contents ix ROS in immunity and inflammation 148 5.1 Mitochondrial ROS in immunity and inflammation 148 5.2 NOX2-derived ROS in immunity and inflammation 150 Outlook 152 Acknowledgments153 Glossary of Acronyms and Abbreviations 153 References155 Chapter 5 Leukocyte Adhesion 171 Klaus Ley and Zhichao Fan Leukocyte adhesion molecules 172 1.1 Integrins 172 1.1.1 Endothelial ligands for integrins 180 1.1.2 ECM ligands for integrins 181 1.2 Selectins 181 1.3 Leukocyte ligands for selectins 182 1.4 Immunoglobulin adhesion molecules 183 184 Biomechanics of leukocytes adhesion under flow 186 Adhesion cascade 3.1 Deviations from the adhesion cascade 187 188 Leukocyte subsets 190 Leukocyte adhesion in lymphatics 190 Leukocyte adhesion to thrombi 191 Defects in leukocyte adhesion References192 Neutrophil Extracellular Traps Chapter 6 205 Tobias A Fuchs, Abdul Hakkim and Constantin F Urban Introduction 1.1 Introduction of neutrophils 1.2 Discovery of NETs Architecture and composition of NETs b3151_FM.indd 205 206 207 208 06-Mar-18 10:00:07 AM ... cM) TNFRSF16 BCMA 16 pl3 .1 ch16(B3) TNFRSF17 AITR, GITR 1p36.3 ch4(E) TNFRSF18 RELT 11 q13.2 unknown TNFRSF19L TROY, TAJ 13 q12 .11 -q12.3 ch14 TNFRSF19 EDAR 2q 11- q13 ch10 EDAR1 EDA2R Xq 11. 1 chX EDA2R... ch17 TNFRSF12A TRAMP, DR3, LARD 1p36.3 ch4 (E1) TNFRSF25 TACI 17 p 11. 2 ch 11 TNFRSF13B BAFFR 22q13 .1- q13. 31 ch15 TNFRSF13C HVEM, HveA, ATAR 13 6.3-p36.3 ch4 TNFRSF14 P75NTR, NGFR 17 q12-q22 ch 11. .. 8p22-p 21 ch14(D1) TNFRSF10B TRALLR3, DcRl 8p22-p 21 ch7 (69.6 cM) TNFRSF10C TRAILR4, DcR2 8p 21 ch7 (69.6 cM) TNFRSF10D RANK, TRANCE-R 18 q22 .1 ch1 TNFRSF11A OPG, TR1 8q24 ch15 TNFRSF11B FN14 16 p13.3