Note: Intro -- Foreword -- Helicobacter pylori, the Gastric Bacterium Which Still Infects Half the World´s Population, Is an Important Part of Gastroente... -- Contents -- Part I: Bacteriology and Molecular Biology -- Chapter 1: Helicobacter pylori: Genetics, Recombination, Population Structure, and Human Migrations -- 1.1 Introduction -- 1.2 The Coevolution of Helicobacter pylori and Humans -- 1.2.1 H. pylori´s Housekeeping Genes -- 1.2.2 Geographic Clustering of Housekeeping Gene Sequences -- 1.2.2.1 Recent Human Population Movements -- 1.2.2.2 Prehistoric Human Migrations -- Bantu speakers: hpAfrica1 -- Nilo-Saharan speakers: hpNEAfrica -- Australians and New Guineans: hpSahul -- Central and Southeast Asians: hpAsia2 -- Native Americans, Han Chinese, and the Austronesians: hpEastAsia -- 1.2.3 Formal Comparisons with Human DNA Data -- 1.2.4 Recombination and Its Effect on Evolutionary Inference -- 1.2.4.1 Population Trees -- 1.2.4.2 The Linkage Model: The Concept of Ancestral Populations -- 1.2.5 Enter Coalescence -- 1.2.5.1 The Global H. pylori Phylogeny -- 1.2.5.2 Age of the H. pylori Human Association -- 1.2.5.3 Sahul Was Colonized Only Once -- 1.2.5.4 The Austronesian Expansion -- 1.2.5.5 San Hunter-Gatherers Are the Original Hosts of hpAfrica2 -- 1.2.5.6 A Second More Recent Out-of-Africa Migration -- 1.2.5.7 Pygmy Hunter-Gatherers Contracted H. pylori Recently from Neolithic Bantus -- 1.2.6 Outlook: Genomics, Aboriginal Populations, and Ancient DNA -- References -- Chapter 2: Adaptation of Helicobacter pylori Metabolism to Persistent Gastric Colonization -- 2.1 Introduction -- 2.2 H. pylori Facing Acidity -- 2.2.1 The Dangers of Low pH -- 2.2.2 Acid Adaptation and Acclimation of H. pylori to the Gastric Niche -- 2.2.3 Establishing the Response to Acidity -- 2.3 Urease, the Major Player in H. pylori Resistance to Acidity. , 2.3.1 Urease Enzymatic Activity -- 2.3.2 Acid-Gated Transport of Urea by the UreI Channel -- 2.3.3 Regulation of the Expression of the Urease Genes -- 2.3.4 Role of the Carbonic Anhydrases in H. pylori -- 2.4 Ammonia Metabolism in H. pylori -- 2.4.1 Minimalist Pathways for Nitrogen Assimilation -- 2.4.2 Central Role of Glutamine Synthetase in Ammonia Metabolism and Possible Coupling with Urease -- 2.4.3 Transport and Metabolism of Amidated Amino Acids -- 2.4.3.1 Asp/Asn and Glu/Gln Uptake in H. pylori -- 2.4.3.2 Asparagine and Glutamine in Translation -- 2.4.3.3 How Are Asn-tRNA and Gln-tRNA Generated in H. pylori? -- 2.4.3.4 The AmiE and AmiF Aliphatic Amidases -- 2.5 Metabolic Enzymes Involved in Virulence -- 2.5.1 Asparaginase -- 2.5.2 Arginase -- 2.6 Metabolism of Nickel, an Essential Metal for the Virulence of Helicobacter pylori -- 2.6.1 Nickel Is a Virulence Determinant for H. pylori -- 2.6.2 Nickel Transport and Efflux -- 2.6.3 Nickel Chaperones and Storage Proteins -- 2.6.3.1 Role of HspA, the Helicobacter-Specific GroES Homolog -- 2.6.3.2 Hpn and Hpn-2: Two Remarkable Histidine-Rich Proteins -- 2.6.4 Urease and Hydrogenase Maturation -- 2.6.4.1 Urease Maturation -- 2.6.4.2 Hydrogenase Maturation -- 2.6.4.3 A Molecular Cross Talk Between Urease and Hydrogenase Maturation Machineries -- 2.7 Conclusions and Outlook -- References -- Chapter 3: Virulence Mechanisms of Helicobacter pylori: An Overview -- 3.1 Introduction -- 3.2 H. pylori Colonisation and Adherence -- 3.2.1 Escape from the Stomach Lumen -- 3.2.2 Adhesion of H. pylori to Gastric Epithelial Cells -- 3.3 Major H. pylori Virulence Factors Involved in Pathogenesis -- 3.3.1 cag Pathogenicity Island (cagPAI) -- 3.3.2 Vacuolating Cytotoxin VacA -- 3.3.3 Other Putative Autotransporter Proteins of H. pylori -- 3.3.4 gamma-Glutamyl Transpeptidase. , 3.3.5 High Temperature Requirement A (HtrA) Serine Protease -- 3.3.6 Other Pro-inflammatory Virulence Factors of H. pylori -- 3.4 Avoidance and Modulation of the Host Immune Response -- 3.4.1 Evasion of Detection by the Innate Immune System -- 3.4.2 Modulation of Phagocytosis and Neutrophil Function -- 3.4.3 Inhibition of Lymphocyte Proliferation -- 3.4.4 Skewing of Adaptive Immune Responses Toward Tolerogenicity -- 3.5 Mitigation of Inflammatory Responses -- 3.6 Modulation of Apoptosis and Autophagy by H. pylori -- 3.6.1 Apoptosis -- 3.6.2 Autophagy -- 3.7 Conclusions and Outlook -- References -- Chapter 4: Roles of the cagPAI and CagA on Gastroduodenal Diseases -- 4.1 Introduction -- 4.2 The cagPAI Encodes a Type IV Secretion System -- 4.3 Crystal Structures of cagPAI Proteins -- 4.4 Pathological Function of the cagPAI Type IV Secretion System -- 4.5 Phosphorylation-Dependent Host Cell Signaling of Translocated CagA -- 4.6 Phosphorylation-Independent Signaling of CagA -- 4.7 T4SS-Dependent but CagA-Independent Cellular Signaling Induced by H. pylori -- 4.8 Conclusions -- References -- Chapter 5: Helicobacter pylori Vacuolating Toxin -- 5.1 Introduction -- 5.2 The vacA Gene vacA Transcription -- 5.3 Secretion and Proteolytic Processing of VacA -- 5.4 Properties of the 88kDa Secreted VacA Protein -- 5.5 VacA Allelic Diversity and Association of vacA Genotypes with Disease -- 5.6 Membrane Channel Formation by VacA -- 5.7 VacA Interactions with Host Cells: Binding, Uptake, and Trafficking -- 5.7.1 Intracellular Actions of VacA -- 5.7.2 Interactions of VacA with the Epithelial Cell Surface -- 5.7.3 Uptake of VacA into an Intracellular Compartment -- 5.7.4 VacA Trafficking to Mitochondria -- 5.7.5 VacA Uptake and Trafficking in Immune Cells -- 5.8 Effects of VacA on Host Cells In Vitro -- 5.8.1 VacA as a Modulator of Epithelial Cell Function. , 5.8.1.1 Alterations in Endosomal Compartments -- 5.8.1.2 Autophagy -- 5.8.1.3 Cell Death -- 5.8.1.4 Alterations in Mitochondria -- 5.8.1.5 Effects of VacA on Cellular Signal Transduction Pathways -- 5.8.1.6 Effects of VacA on Epithelial Cell Permeability and the Cytoskeleton -- 5.8.2 VacA as a Modulator of Immune Cell Function -- 5.8.2.1 Effects of VacA on T and B Lymphocytes -- 5.8.2.2 Effects of VacA on Other Types of Immune Cells -- 5.8.3 Effects of VacA on Parietal Cells and Acid/Base Balance -- 5.9 Synergistic and Antagonistic Associations Between VacA and CagA -- 5.10 Role of VacA In Vivo -- 5.10.1 Role of VacA in H. pylori Colonization of the Stomach -- 5.10.2 Role of VacA in Gastroduodenal Disease -- 5.11 Conclusions and Outlook -- References -- Chapter 6: Roles of the BabA and the SabA Adhesins in Gastroduodenal Diseases -- 6.1 Introduction -- 6.2 The Blood Group Antigen-Binding Adhesin BabA -- 6.2.1 Identification of the Blood Group Antigen-Binding Adhesin BabA -- 6.2.2 Location of the babA Gene -- 6.2.3 Mechanisms That Switches BabA Expression On and Off -- 6.2.4 Regulation of BabA Expression Levels -- 6.2.5 BabA Expression and Gastric Disease -- 6.3 The Sialic Acid-Binding Adhesin SabA -- 6.3.1 H. pylori Binding to the Inflammation-Associated Sialyl-Lewis x/a Antigen Receptor -- 6.3.2 Identification of the Sialic Acid-Binding Adhesin SabA -- 6.3.3 The SabA Adhesin Is the H. pylori Hemagglutinin -- 6.3.4 Mechanisms for Regulation of SabA Expression -- 6.3.5 SabA Expression and Regulation by Acidic Conditions -- 6.3.6 SabA and Gastroduodenal Diseases -- 6.4 BabA- and SabA-Mediated Binding to Mucins -- 6.5 BabA- and SabA-Mediated Adhesion of H. pylori Outer Membrane Vesicles to the Gastric Mucosa -- 6.6 Conclusion and Outlook -- References -- Chapter 7: Emerging Novel Virulence Factors of Helicobacter pylori -- 7.1 Introduction. , 7.2 The Effects of GGT on Epithelial Cells and Immune Cells -- 7.3 NapA Affects the Host Immune System -- 7.4 Tipα: A Multifunctional Factor? -- 7.5 JHP0940 Encodes the Bacterial Kinase CtkA -- 7.6 Helicobacter pylori Secretes Proteases That Target Host Cell Proteins with Important Functions in Pathogenesis -- 7.7 HtrA Can Affect H. pylori Pathogenesis via Direct Cleavage of E-Cadherin and Fibronectin -- 7.8 The Helicobacter Outer Membrane Proteins HopQ and HopZ Contribute to Bacterial Adherence -- 7.9 DupA as a Marker for H. pylori-Associated Disorders -- 7.10 Conclusions and Outlook -- References -- Chapter 8: The Primary Transcriptome and Noncoding RNA Repertoire of Helicobacter pylori -- 8.1 Introduction -- 8.2 Primary Transcriptome Analysis of Helicobacter pylori -- 8.2.1 Bacterial Transcriptome Analysis Using RNA-Seq -- 8.2.2 Differential RNA-Seq for Primary Transcriptome Analysis -- 8.3 Helicobacter Transcriptome Features Identified by dRNA-Seq -- 8.3.1 Global Transcriptional Start Site Maps -- 8.3.2 5 UTR Lengths -- 8.3.3 Operon and Suboperon Structure -- 8.3.4 Noncoding RNAs -- 8.3.4.1 Housekeeping RNAs -- 8.3.4.2 Mechanisms and Functions of Antisense/Base-Pairing RNAs in H. pylori -- Trans-Encoded Antisense RNAs -- Cis-Encoded Antisense RNAs -- 8.3.5 Class I Toxin-Antitoxin Loci -- 8.4 Protein Factors Involved in Posttranscriptional Regulation -- 8.4.1 RNA-Binding Proteins -- 8.4.2 Ribonucleases -- 8.5 Conclusions and Outlook -- References -- Chapter 9: Genome Evolution: Helicobacter pylori as an Extreme Model -- 9.1 Prologue -- 9.2 Phylogeny and Population Structure -- 9.2.1 Genome Trees vs. Gene Trees -- 9.2.2 Inference of Population Structure from Mutual Homologous Recombination -- 9.3 Evolution of Individual Genes -- 9.3.1 The cagA Oncogene -- 9.3.2 Decay of Molybdenum-Related Genes -- 9.3.3 Outer Membrane Proteins. , 9.4 Evolution of Chromosome Synteny.

Note: Intro -- Foreword -- Contents -- Abbreviations -- Human Campylobacteriosis-A Serious Infectious Threat in a One Health Perspective -- 1 Introduction -- 2 The One Health Concept: General Theory and Practical Approaches -- 3 Human Campylobacteriosis-From Clinical Investigations to Novel Treatment Options Using Innovative Murine Models of Infection -- 3.1 Human Campylobacteriosis-Basic Characteristics -- 3.2 Burden of Disease -- 3.3 Molecular Concepts of C. jejuni-Induced Intestinal Pathogenesis -- 3.4 Novel Murine Models of C. jejuni Infection Offering Detailed Investigations and Treatment Strategies for Campylobacteriosis and Associated Long-Term Sequelae -- 4 Concluding Remarks -- References -- The Data Behind Risk Analysis of Campylobacter Jejuni and Campylobacter Coli Infections -- 1 Introduction -- 2 Risk Assessment of Human Campylobacteriosis -- 2.1 Hazard Identification -- 2.2 Hazard Characterization -- 2.3 Exposure Assessment -- 2.4 Risk Characterization -- 3 Current Surveillance Strategies of Campylobacter -- 4 Risk Management -- 4.1 Control in Poultry Meat -- 4.2 Control of Campylobacter Sources Other Than Poultry Meat -- 5 Risk Communication -- 6 Concluding Remarks -- References -- Population Biology and Comparative Genomics of Campylobacter Species -- 1 Introduction -- 2 Evolution Theory and Concepts for the Genus Campylobacter -- 3 Population Structure -- 3.1 Diversity and Population Structure of C. Jejuni and C. Coli -- 3.2 Inter Species Recombination and Hybrid Species -- 3.3 Additional Species -- 4 Host Association of Campylobacter -- 4.1 Impact of Genomic High-Throughput Methods -- 4.2 Source Attribution in Clinical and Agricultural Setting -- 4.3 Relevance for Public Health (Applications) -- 5 Concluding Remarks -- References. , Management Strategies for Prevention of Campylobacter Infections Through the Poultry Food Chain: A European Perspective -- 1 Introduction -- 2 Management Practices and Control Options -- 2.1 Farm Level -- 2.2 Abattoir Level -- 2.3 Post-harvest Level -- 2.4 Retail and Consumer Phase -- 2.5 Management and Responsibilities -- 3 Concluding Remarks -- References -- Emission Sources of Campylobacter from Agricultural Farms, Impact on Environmental Contamination and Intervention Strategies -- 1 Introduction -- 2 Colonization of Campylobacter in Livestock -- 3 Emission Sources -- 3.1 Manure -- 3.2 Air -- 3.3 Insects and Rodents -- 3.4 Personnel, Equipment, Vehicles -- 3.5 Waterborne Emission -- 4 Tenacity of Campylobacter in the Environment -- 5 Viable but Non-culturable Form of Campylobacter in the Environment -- 6 Intervention Against Emission -- 7 Concluding Remarks -- References -- Phage Biocontrol of Campylobacter: A One Health Approach -- 1 Introduction -- 2 Campylobacter Bacteriophages in a One Health Approach -- 3 Interactions of Bacteria with Their Bacteriophages and the Development of Resistance -- 4 Phage Treatment of Campylobacter in the Literature -- 4.1 Experimental Phage Treatment of Contaminated Meat -- 4.2 Experimental Phage Treatment of Colonized Chickens -- 5 Practical Hurdles and Open Questions that Need to Be Addressed -- 6 Resistance of Campylobacter Phages -- 7 Regulatory Aspects and Safety of Campylobacter Bacteriophages -- 8 Concluding Remarks -- References -- Campylobacter Virulence Factors and Molecular Host-Pathogen Interactions -- 1 Introduction -- 2 Bacterial Virulence Factors and Epithelial Cell Responses -- 2.1 Specialized Metabolism and Enteric Life Style -- 2.2 Campylobacter Motility and Chemotaxis -- 2.3 CDT Toxin Production -- 2.4 Serine Protease HtrA and Epithelial Barrier Disruption. , 2.5 Outer Membrane Adhesins and Host Cell Binding -- 2.6 The Flagellum as a Specialized Type III Secretion System -- 2.7 Bacterial Factors and Signaling Involved in Host Cell Invasion -- 2.8 Intracellular Survival and Trafficking of Campylobacter -- 3 Bacterial Virulence Factors and Immune Cell Responses -- 3.1 Interaction with Toll-Like Receptors -- 3.2 Role of Siglec Receptors -- 3.3 Activation of the NLRP3 Inflammasome -- 4 Concluding Remarks -- References -- Diarrheal Mechanisms and the Role of Intestinal Barrier Dysfunction in Campylobacter Infections -- 1 Introduction -- 2 Pathogenetic Principles and Diarrheal Mechanisms in campylobacteriosis -- 2.1 Barrier Dysfunction, Leak Flux and Leaky Gut -- 2.2 Immune Cell Response and Barrier Function -- 3 Barrier Dysfunction in Campylobacter Infection -- 3.1 Barrier Defects by C. jejuni, C. coli, C. fetus, C. concisus and Related Bacteria -- 3.2 Protective Approaches -- 4 Concluding Remarks -- References -- Murine Models for the Investigation of Colonization Resistance and Innate Immune Responses in Campylobacter Jejuni Infections -- 1 Introduction -- 2 Factors Affecting Campylobacter Colonization and Infection -- 3 Susceptibility to Lipooligosaccharide Determines Host Specificity of Campylobacter Colonization Versus Infection -- 3.1 Chickens -- 3.2 Mice -- 3.3 Humans -- 4 Murine Infection Models in Campylobacteriosis Research -- 4.1 Germfree and Secondary Abiotic Mice -- 4.2 Human Microbiota-Associated Mice -- 4.3 Infant Mice -- 4.4 Zinc-Deficient Mice -- 4.5 SIGIRR-Deficient Mice -- 4.6 IL-10 Deficient Mice -- 5 Concluding Remarks -- References -- Natural Competence and Horizontal Gene Transfer in Campylobacter -- 1 Introduction -- 2 Mechanisms of Horizontal Gene Transfer -- 2.1 Natural Transformation and Uptake of Free DNA -- 2.2 Conjugative Gene Transfer. , 2.3 Phage Transduction and Genomic Rearrangements -- 3 Barriers to Horizontal Gene Transfer -- 3.1 CRISPR-Cas and Nucleases -- 3.2 Methylation-Dependent DNA Recognition -- 4 Impact of Gene Transfer on Campylobacter Fitness -- 4.1 Spread of Resistomes and Persistence Factors -- 4.2 Interspecies Gene Transfer -- 5 Concluding Remarks -- References -- Molecular Mechanisms of Campylobacter Biofilm Formation and Quorum Sensing -- 1 Introduction -- 2 Microbial Biofilm Formation -- 2.1 Building and Dispersion of Microbial Biofilms -- 2.2 Methods to Analyse Biofilms -- 2.3 Environmental Conditions Influencing Campylobacter jejuni Biofilm Formation -- 2.4 Genetic Background and Genes Impacting Biofilm Formation of C. jejuni -- 2.5 Control Strategies Targeting C. jejuni Biofilms -- 3 Quorum Sensing -- 3.1 Quorum Sensing Signalling Mechanisms -- 3.2 Phenotypes of C. jejuni luxS Mutants -- 3.3 Quorum Quenching -- 4 Concluding Remarks -- References -- Correction to: Fighting Campylobacter Infections -- Correction to: S. Backert (ed.), Fighting Campylobacter Infections, Current Topics in Microbiology and Immunology 431, https://doi.org/10.1007/978-3-030-65481-8.