Bacterial Evasion of Host Immune Responses (Advances in Molecular and Cellular Microbiology, Series Number 2)

Over the past fifty years cells and mediators involved in our immune defences have been painstakingly identified. However, it is only relatively recently that the ability of microorganisms to evade immunity has been recognized and investigated. This volume introduces the mechanisms used by bacteria to evade both humoral and cellular immune responses, using systems ranging in complexity from the simple quorum sensing molecules (acyl homoserine lactones) to the supramolecular syringe-like devices of type III secretion systems. Half-title......Page 3 Series-title......Page 4 Title......Page 5 Copyright......Page 6 Contents......Page 7 Contributors......Page 9 Preface......Page 17 PART I Recognition of bacteria......Page 19 1.2.1 The dendritic cell family......Page 21 1.2.2 Relationship between dendritic cells and macrophages......Page 24 1.3 DENDRITIC CELLS AND BACTERIAL IMMUNE RESPONSES......Page 26 1.3.2 Toll-like receptors (TLRs) and bacterial recognition......Page 27 1.3.3 How do dendritic cells process bacterial antigens?......Page 28 1.3.4 Dendritic cells as a means of bacterial invasion – sentinels or Trojan horses?......Page 29 1.4 DENDRITIC CELLS AND THE GUT FLORA – A PARADOX?......Page 30 1.5 CONCLUSION......Page 31 REFERENCES......Page 32 2.2 EVOLUTION OF CD1......Page 39 2.3 TISSUE DISTRIBUTION OF CD1......Page 40 2.5 CD1 AND ANTIGEN PRESENTATION......Page 41 2.6 CD1-RESTRICTED T LYMPHOCYTES......Page 44 2.7 CD1 AND ANTIGEN INTERACTION......Page 45 2.9 INTRACELLULAR TRAFFICKING OF CD1......Page 46 2.10 CD1 AND MYCOBACTERIAL INFECTIONS......Page 48 2.11 CONCLUSION......Page 50 REFERENCES......Page 51 3.2 EARLY WORK ON Bcg......Page 57 3.3 REVERSE GENETICS APPROACH TO CLONING Nramp1......Page 58 3.4 DEMONSTRATION THAT Nramp1 IS Bcg......Page 59 3.6 THE Nramp FAMILY......Page 60 3.7 Nramp PROTEINS AND METAL CATION TRANSPORT......Page 61 3.8 Nramp AND HUMAN SUSCEPTIBILITY TO INTRACELLULAR PATHOGENS......Page 63 ACKNOWLEDGMENTS......Page 64 REFERENCES......Page 65 PART II Evasion of humoral immunity......Page 71 4.1 INTRODUCTION......Page 73 4.2 BIOLOGICAL FUNCTIONS OF THE COMPLEMENT SYSTEM......Page 75 4.3 THE INVOLVEMENT OF THE COMPLEMENT SYSTEM IN ANTI-BACTERIAL DEFENCES......Page 78 4.4 BACTERIAL EVASION OF THE COMPLEMENT SYSTEM......Page 80 4.5 BACTERIAL CELL SURFACES AND COMPLEMENT ACTIVATION......Page 83 4.6 BACTERIAL PROTEINASES AND ANAPHYLATOXINS......Page 84 4.7 EVASION USING RCA PROTEINS......Page 85 4.8 TARGETING THE LYTIC PATHWAY......Page 87 4.9 UTILISATION OF THE COMPLEMENT SYSTEM......Page 88 REFERENCES......Page 89 5.2 IgA PROTEASE-PRODUCING BACTERIA......Page 99 5.3 CONVERGENT EVOLUTION OF IgA PROTEASES......Page 101 5.4 SPECIFIC ADAPTATION TO HOST AND HABITAT......Page 103 5.5 IN VIVO ACTIVITY......Page 104 5.6 BIOLOGICAL SIGNIFICANCE OF IgA CLEAVAGE......Page 106 5.7 ALTERNATIVE SUBSTRATES AND FUNCTIONS OF IgA PROTEASES......Page 108 5.9 OTHER MICROBIAL PROTEASES WITH IMMUNOGLOBULIN-CLEAVING ACTIVITY......Page 109 5.10 EFFECTS OF BACTERIAL GLYCOSIDASES......Page 110 5.11 Ig-BINDING PROTEINS......Page 111 5.12 CONCLUSION......Page 112 REFERENCES......Page 113 6.2 SECTION 1: PHASE VARIATION, ITS CHARACTERISTICS AND HOW IT WORKS......Page 121 6.2.1 The capacity to generate diversity......Page 124 6.2.2 Stability in the presence of instability......Page 125 6.3.1 Phase variation in Borrelia......Page 126 6.3.2 The association between phase variation and antigenic variation......Page 127 6.3.3 Haemophilus LPS variation in vivo......Page 129 6.3.4 Neisseria meningitidis and Neisseria gonorrhoeae......Page 131 6.4 CONCLUSION......Page 134 REFERENCES......Page 135 PART III Evasion of cellular immunity......Page 143 7.1 INTRODUCTION......Page 145 7.2 TYPE III SECRETION SYSTEMS......Page 146 7.3 SECRETION AND DELIVERY OF EFFECTOR PROTEINS BY YERSINIA AND P.AERUGINOSA......Page 147 7.4 ROLE OF TYPE III SECRETION SYSTEMS IN BACTERIAL INFECTIONS......Page 150 7.4.1 P.aeruginosa infections......Page 152 7.4.2 Yersinia infections......Page 153 7.5 INHIBITION OF PHAGOCYTOSIS......Page 154 7.6.1 The Yersinia effector YopH......Page 156 7.6.2 Role of the YopH targets in normal cell function......Page 158 7.6.3 Immediate early targeting of focal complex structures by YopH......Page 160 7.7 SptP OF SALMONELLA......Page 161 7.8.1 Yersinia effectors interfering with Rho GTPases......Page 163 7.8.2 The Yersinia effector YopE......Page 164 7.8.3 The Pseudomonas aeruginosa effectors Exoenzyme S and T......Page 166 7.8.4 SptPof Salmonella......Page 169 7.9 CONCLUSIONS......Page 171 REFERENCES......Page 172 8.1 INTRODUCTION......Page 189 8.2.1 Superantigens stimulate T cells via the Vbeta-region of TcR......Page 192 8.3 SAGs REQUIRE MHC CLASS II FOR FUNCTION......Page 193 8.3.1 The staphylococcal and streptococcal SAG family......Page 194 8.5 ALLELIC VARIATION OF SAGs IN STREPTOCOCCUS PYOGENES......Page 196 8.6 SAGs FROM OTHER BACTERIA......Page 197 8.7.1 Mouse mammary tumor virus......Page 198 8.7.3 Cytomegalovirus (CMV)......Page 199 8.8.2 Staphylococcal food poisoning......Page 200 8.8.3 Toxic Shock Syndrome......Page 201 8.8.5 Streptococcal throat and rheumatic fever......Page 202 8.8.7 SAGs in autoimmune diseases......Page 203 8.9 THE STRUCTURE AND FUNCTION OF THE STAPHYLOCOCCAL AND STREPTOCOCCAL SUPERANTIGENS......Page 204 8.10 HOW DO SAGs BIND TO THE TcR?......Page 208 8.11 SAG STIMULATION OF T CELLS......Page 209 8.12 WHAT IS THE FUNCTION OF SAGs?......Page 210 REFERENCES......Page 211 Abbreviations and nomenclature.......Page 219 9.2 COMPARTMENTALISED IMMUNE RESPONSES TO PATHOGENIC ORGANISMS......Page 220 9.3.1 Quorum sensing networks in Pseudomonas aeruginosa......Page 223 9.5 QSMs AND IMMUNITY TO PSEUDOMONAS AERUGINOSA......Page 225 9.6 CONCLUSION......Page 233 REFERENCES......Page 234 10.1 INTRODUCTION......Page 241 10.2 CYTOKINE NETWORKS......Page 242 10.3 BACTERIA AND CYTOKINE NETWORKS......Page 246 10.4 THE NORMAL MICROBIOTA AND THE COMMENSAL PARADOX......Page 248 10.5 BACTERIAL EVASION OF PROTECTIVE PRO-INFLAMMATORY CYTOKINE NETWORKS......Page 249 10.6 MICROBIAL INHIBITION OF PRO-INFLAMMATORY CYTOKINE NETWORKS......Page 250 10.6.1 Bacterial proteins or mechanisms inhibiting cytokine synthesis......Page 251 10.6.2 Bacterial proteinases and cytokine inactivation/activation......Page 252 10.6.3 Bacterial receptors for cyokines......Page 254 10.7 CONCLUSION......Page 255 REFERENCES......Page 256 11.1 INTRODUCTION......Page 261 11.2.1 Introduction......Page 263 11.2.2 Effect of CT on antigen-presenting cells......Page 264 11.2.3 Effect of CT on T lymphocytes......Page 265 11.2.4 Effect of CT in vivo......Page 267 11.2.5 Clinical application of CT......Page 269 11.2.6 Summary......Page 270 11.3.1 Introduction......Page 271 11.3.3 Effect of LT on T cells......Page 272 11.3.4 Effect of LT in vivo......Page 273 11.3.5 Clinical application of LT......Page 274 11.4.1 Introduction......Page 275 11.4.3 Effect of Stx on mixed mononuclear cell populations......Page 276 11.4.5 Summary......Page 277 11.5.2 Effect of C. difficile toxins on antigen-presenting cells......Page 278 11.5.3 Effect of C. difficile toxins in vivo......Page 279 11.6.2 Effect of lymphostatin on T cells......Page 280 11.6.4 Summary......Page 281 REFERENCES......Page 282 12.1 INTRODUCTION......Page 297 12.2 TRANSCRIPTION FACTOR NF-KappaB: THE MASTER REGULATOR OF THE HOST IMMUNE RESPONSE......Page 298 12.3 TARGETING OF THE NF-KappaB PATHWAY BY PATHOGENIC AND NONPATHOGENIC BACTERIA IN THE GUT......Page 300 12.4 THE YERSINIA TYPE III PROTEIN SECRETION MACHINERY: A PROTOTYPICAL TOOL FOR SUBVERTING THE PHAGOCYTE......Page 301 12.5 SUPPRESSION OF THE HOST CELL CYTOKINE PRODUCTION......Page 303 12.6 TRIGGERING MACROPHAGE CELL DEATH BY APOPTOSIS......Page 304 12.7 IS YopP/J A UNIQUE BACTERIAL EFFECTOR PROTEIN?......Page 307 REFERENCES......Page 308 Index......Page 313

comprehensive Review Of Current Research Concerning How Bacteria Evade Immunity And Hence Cause Infection.

doody Review Services

reviewer:eugene A Davidson, Phd(georgetown University School Of Medicine)
description:this Book Contains A Series Of Reviews On The Mechanisms Used By Bacteria To Evade Immune Responses In Mammalian Hosts. Humoral And Cellular Responses Are Considered, Including Those Mediated By Complement.
purpose:the Intent Is To Provide Current Information Regarding Methods/strategies Used By Bacteria To Abrogate Or Mitigate Host Immune Response. Given The Persistence Of Serious Infectious Disease, This Is A Worthwhile Endeavor. Within Limitations, These Expectations Are Fulfilled.
audience:the Target Audience Is The Medical Scientist (including Basic Investigators) Concerned With Molecular Mechanisms Of Virulence And Disease. The Editors Have Assembled A Highly Qualified Set Of Authors
features:most Concerns Regarding Bacterial Infection Relate To Identifying Which Antibiotic Will Be Effective For Therapeutic Intervention. Generally, Less Attention Is Focused On The Fact That The Infection Is Well Established Before Overt Symptoms Occur That Can Lead To Such Treatment, And That Substantial Interchange Between The Invading Organism And The Host Immune System Has Already Occurred. This Book Focuses On The Latter Aspect. The Initial Chapters Review Mechanisms Of Host Recognition Of Bacteria And Is Followed By Two Main Sections That Deal With Humoral And Cell Mediated Responses. In Each Of These Latter Parts, Several Different Aspects Are Reviewed. These Include The Role Of The Complement System, Elicited Proteins That Bind Immunoglobulins And What Is Termed Phase Variation. This Latter Is Analogous To The Strategy Employed By Trypanosomes Wherein A Set Of Coat Protein Genes Is Available To Provide A Constantly Changing Exterior Landscape Thus Obviating Immune Responses. In The Final Section, Cellular Responses Are Discussed -- Thus, Signaling Networks, The Role Of Superantigens And Enterotoxins And Quorum Sensing Are All Discussed In Terms Of Their Effects On The Host Cellular Response. In General, The Discussions Are Thorough With A Strong Molecular Emphasis. The Bibliographies Are Sufficiently Detailed To Provide Adequate Primary Material. There Are, However, Some Caveats. The Overall Topic Is Hardly Restricted To Bacterial Infections. Thus, Strategies Employed By Parasites, In Particular, May Have Deserved Mention. In The Discussion Of Bacterial Capsules, No Distinction Is Made Between That Of Hemolytic Streptococci (non-immunogenic Hyaluronic Acid) And Those Where A Strong Immune Response Can Be Expected And Where The Capsular Material Itself Can Serve As A Protective Immunogen (streptococcus Pneumoniae, For Example). Overall, This Book Is Recommended For Those Investigators Concerned With Aspects Of Bacterial Infectious Disease.
assessment:this Is A Generally Useful Book. Investigators With A Broad Concern For Infectious Processes Will Find Much Of Value But Will Miss Comparable Discussions Of Parasites And Viruses. The Book Is Timely And Not Especially Duplicative.

Our survival as multicellular organisms requires the constant surveillance of our internal and external (mucosal) environments by the multifarious elements of the innate and acquired systems of immunity. The objective of this surveillance, expensive as it is to the organisms, is to recognise and kill invading microorganisms. Over the past fifty years the cells and mediators involved in our immune defences have been painstakingly identified. However, it is only relatively recently that the ability of microorganisms to evade immunity has been recognised and investigated. Bacterial Evasion of Host Immune Responses introduces the reader to the mechanisms used by bacteria to evade both humoral and cellular immune responses, using systems ranging in complexity from the simple quorum sensing molecules - acyl homoserine lactones - to the supramolecular syringe-like devices of type III secretion systems. This book will be of interest to researchers and graduate students in microbiology, immunology, pharmacology and molecular medicine Over the past decade researchers have shown that bacteria have evolved many ways of evading immunity and hence causing infection. Our present understanding of these mechanisms is described in this book, which will appeal to graduate students and researchers in microbiology, immunology, as well as in pharmacology and molecular medicine