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Pseudomonas [[electronic resource] ] : Volume 7: New Aspects of Pseudomonas Biology / / edited by Juan-Luis Ramos, Johanna B. Goldberg, Alain Filloux
| Pseudomonas [[electronic resource] ] : Volume 7: New Aspects of Pseudomonas Biology / / edited by Juan-Luis Ramos, Johanna B. Goldberg, Alain Filloux |
| Edizione | [1st ed. 2015.] |
| Pubbl/distr/stampa | Dordrecht : , : Springer Netherlands : , : Imprint : Springer, , 2015 |
| Descrizione fisica | 1 online resource (319 p.) |
| Disciplina |
579
610 |
| Soggetto topico |
Medicine
Microbiology Biomedicine, general |
| ISBN | 94-017-9555-X |
| Formato | Materiale a stampa  |
| Livello bibliografico | Monografia |
| Lingua di pubblicazione | eng |
| Nota di contenuto | Pseudomonas aeruginosa Host Immune Evasion -- Pseudomonas entomophila: a versatile bacterium with entomopathogenic properties -- Pseudomonas Activation of the Inflammasome -- P. aeruginosa type VI secretion machinery: another deadly syringe -- Anaerobic life style of Pseudomonas aeruginosa -- Pseudomonas strains that exert biocontrol of plant pathogens -- Resistance and response to anti-pseudomonas agents and biocides -- Lessons from the QSCR structure for Quorum sensing -- Understanding and Exploiting Bacterial Outer Membrane Vesicles -- Events in root colonization by Pseudomonas putida -- My memories of Pseudomonas in the twentieth century. |
| Record Nr. | UNINA-9910298282403321 |
| Dordrecht : , : Springer Netherlands : , : Imprint : Springer, , 2015 | ||
| Materiale a stampa | ||
| Lo trovi qui: Univ. Federico II | ||
| ||
Pseudomonas aeruginosa : biology, pathogenesis and control strategies / / Alain Filloux, Juan-Luis Ramos, editors
| Pseudomonas aeruginosa : biology, pathogenesis and control strategies / / Alain Filloux, Juan-Luis Ramos, editors |
| Pubbl/distr/stampa | Cham, Switzerland : , : Springer, , [2022] |
| Descrizione fisica | 1 online resource (452 pages) |
| Disciplina | 616.0145 |
| Collana | Advances in experimental medicine and biology |
| Soggetto topico |
Pseudomonas aeruginosa infections
Gram-negative bacterial infections Lungs - Infections |
| ISBN | 3-031-08491-8 |
| Formato | Materiale a stampa |
| Livello bibliografico | Monografia |
| Lingua di pubblicazione | eng |
| Nota di contenuto |
Intro -- Preface -- Contents -- Contributors -- Part I: Biology and Evolution of Pseudomonas aeruginosa -- 1: Pseudomonas aeruginosa Pangenome: Core and Accessory Genes of a Highly Resourceful Opportunistic Pathogen -- 1.1 Pseudomonas aeruginosa Environment and Main Genomic Characteristics -- 1.1.1 Pangenomics and Populations Structure Analyses in Population Genomics -- 1.2 The Population Structure of Pseudomonas aeruginosa -- 1.3 The Pangenome of Pseudomonas aeruginosa -- 1.3.1 Characterization of the Core Genome of Pseudomonas aeruginosa -- 1.3.2 Comparison of Antibiotic Resistance Profiles Among Phylogroups of Pseudomonas aeruginosa Species -- 1.4 The Highly Variable Accessory Genome of Pseudomonas aeruginosa -- 1.5 Conclusions -- References -- 2: Iron Homeostasis in Pseudomonas aeruginosa: Targeting Iron Acquisition and Storage as an Antimicrobial Strategy -- 2.1 Introduction -- 2.2 Iron Acquisition Systems in P. aeruginosa -- 2.2.1 Production and Utilization of the Endogenous Siderophores Pyoverdine and Pyochelin -- 2.2.2 Xenosiderophore-Mediated Iron Acquisition -- 2.2.3 Iron Acquisition from the Host Heme Molecule -- 2.2.4 Fe2+ Acquisition by the Feo System -- 2.2.5 Iron Acquisition Mediated by PQS Molecule and TseF -- 2.3 Iron Storage Systems in P. aeruginosa -- 2.4 Iron Efflux Systems in P. aeruginosa -- 2.5 Regulation of Iron Homeostasis in P. aeruginosa by General Regulators -- 2.5.1 Iron Sensing and Regulation by the Ferric Uptake Transcriptional Regulator Fur -- 2.5.2 Regulation of Iron Homeostasis by Small RNAs -- 2.6 Siderophore Signaling in the Regulation of Iron Homeostasis -- 2.6.1 Siderophore Signaling by σECF Factors and Cell-Surface Signaling -- 2.6.2 Siderophore Signaling by Two-Component Systems -- 2.6.3 Siderophore Signaling by One-Component Systems.
2.7 Other Systems Involved in the Regulation of Iron Homeostasis in P. aeruginosa -- 2.8 Iron and P. aeruginosa Virulence -- 2.9 Strategies to Block P. aeruginosa Infections by Disrupting Iron Homeostasis -- 2.9.1 Neutralization of Siderophores with Lipocalin-Based Proteins -- 2.9.2 Utilization of Iron Chelators -- 2.9.3 Utilization of the Iron Mimicking Metal Gallium -- 2.9.4 Use of Siderophore-Dependent Uptake Systems to Deliver Antimicrobials: The `Trojan-Horse´ Strategy -- 2.9.5 Other Strategies -- References -- 3: Controlling Biofilm Development Through Cyclic di-GMP Signaling -- 3.1 Introduction -- 3.2 The First Contact with the Surface: Timing and Heterogeneity of Contact-Dependent Modulation of c-di-GMP Levels -- 3.3 Consequences of Surface Contact and Downstream Factors -- 3.4 Key Players Contributing to Biofilm Maturation -- 3.5 c-di-GMP Levels and Maintenance of the Mature Biofilm Structure -- 3.6 Biofilm Dispersion: The Return to Low c-di-GMP Levels -- 3.7 Turnover and Modulation of the c-di-GMP Pool in Biofilms -- 3.8 Blocking c-di-GMP for Biofilm Control -- 3.9 Conclusion -- References -- 4: Pseudomonas aeruginosa Quorum Sensing -- 4.1 History and Introduction to P. aeruginosa Quorum Sensing -- 4.2 QS and Virulence of P. aeruginosa -- 4.3 Ecological and Evolutionary Considerations -- 4.4 Quorum Sensing Inhibition Strategies -- 4.5 A Look Ahead -- References -- 5: Antibiotic Resistance in Pseudomonas -- 5.1 Introduction -- 5.2 Reasons Behind the Intrinsic Low Susceptibility to Antibiotics of P. aeruginosa -- 5.3 Mutational Resistance in P. aeruginosa -- 5.4 Acquisition of Antibiotic Resistance Genes -- 5.5 High-Risk MDR P. aeruginosa Clones -- 5.6 Habitat- and Physiology-Dependent Antibiotic Resistance -- 5.7 Transient Antibiotic Resistance -- 5.8 Tolerance and Persistence -- 5.9 Biofilms -- 5.10 Concluding Remarks -- References. Part II: Cell Envelope and Secretion Systems -- 6: Cell Envelope Stress Response in Pseudomonas aeruginosa -- 6.1 Introduction -- 6.2 The Gram-Negative Cell Envelope -- 6.3 Cell Envelope Stresses in P. aeruginosa -- 6.3.1 Antibiotic Stresses Inducing a CESR -- 6.3.2 Some Examples of Abiotic Stresses Leading to CESR -- 6.3.2.1 Temperature -- 6.3.2.2 Osmolarity -- 6.3.2.3 Mechanical Stresses -- 6.4 Cell Envelope Stress Responses (CESRs) in P. aeruginosa -- 6.4.1 CESR-Related Sigma Factors -- 6.4.1.1 The E. coli σE Homologue AlgU -- 6.4.1.1.1 The Case of Mucoidy -- 6.4.1.2 The Bacillus subtilis SigW ECFσ Homologue SigX -- 6.4.1.2.1 The SigX ECFσ Controls Membrane Homeostasis in P. aeruginosa -- 6.4.1.2.2 Conditions Leading to Increased SigX Expression or Activity -- Absence of the Major Porin OprF -- Hypo-Osmolarity but Not Hyperosmolarity -- Cold Temperature Adaptation -- Sublethal Concentration of Valinomycin -- Super-infective Phage Infection Results in High Expression and Activity of SigX -- 6.4.1.2.3 Conditions Decreasing SigX Expression or Activity -- Absence of CmpX -- Changes in sigX Expression and Activity Caused by Some Plant Metabolites -- 6.4.1.2.4 The Elusive SigX Regulon Definition -- 6.4.1.3 The SbrI ECFσ Factor, Another Cell Wall Stress Regulator? -- 6.4.1.4 Hyperosmolarity Induces the Expression of AlgU-Regulated Genes -- 6.4.1.5 AlgU Is Involved in Heat Shock Response via RpoH Activation -- 6.4.1.6 Low-Shear Modeled Microgravity Involves AlgU, RpoH, and SigX Responses -- 6.4.1.7 Contact with Epithelial Cells Causes an AlgU-Related CESR -- 6.4.1.8 d-Cycloserine Antibiotic Induces an AlgU-Related CESR -- 6.4.1.8.1 d-Cycloserine Activates the AlgU Regulon -- 6.4.1.8.2 DCS Treatment Failed to Trigger Alginate Production Despite Strong AlgU Induction -- 6.4.1.8.3 DCS Exposure Causes Many AlgU-Dependent Transcript Upregulation. 6.4.1.8.4 Many Lipoprotein Genes Are Upregulated upon DCS Exposure -- 6.4.1.8.5 DCS Triggers Expression of Some H1-T6SS Secretion Genes -- 6.4.2 CESR-Related Two-Component Systems -- 6.4.2.1 The AmgRS Two-Component System Is Involved in CESR -- 6.4.2.2 Polymyxin-Induced Adaptative Resistance in Response to CESR -- 6.4.2.3 Response to β-Lactams -- 6.4.3 Mechanosensitive Channels as CESR Actors -- 6.4.3.1 Mechanosensitive Channels as CESR Actors -- 6.5 Concluding Remarks -- References -- 7: Flagella, Chemotaxis and Surface Sensing -- 7.1 Introduction -- 7.2 Flagella -- 7.2.1 The Flagellum Is the Most Complex Protein Assembly in Bacteria -- 7.2.2 PA Contains a Single Polar Flagellum -- 7.2.3 PA Employs a ``Run-Reverse-Turn´´ Chemotaxis Mechanism That Is Different to That of Enterobacteria -- 7.2.4 The Cost of Flagella and Strategies to Reduce It -- 7.2.5 PA Has a Dual Stator Motor -- 7.2.6 Understanding Filament Function -- 7.2.7 The Multiple Roles of Flagella -- 7.2.8 The Flagellum and Its Effect on Virulence and Virulence-Related Phenotypes -- 7.2.9 Flagellar Proteins as Anti-PA Vaccine Antigens or Targets for Antimicrobial Agents -- 7.3 Chemotaxis -- 7.3.1 PA Chemosensory Pathways -- 7.3.2 Core and Auxiliary Proteins of Chemosensory Pathways -- 7.3.3 Canonical Modes of Signal Perception at Chemoreceptors -- 7.3.4 Chemotaxis and the Che Pathway -- 7.3.4.1 Chemotaxis to Histamine and Polyamines -- 7.3.4.2 Chemotaxis to Inorganic Phosphate -- 7.3.4.3 Chemotaxis to Nitrate -- 7.3.4.4 Chemotaxis to Amino Acids -- 7.3.4.5 Chemotaxis to Autoinducer-2 -- 7.3.4.6 Chemotaxis to Organic Acids -- 7.3.4.7 Other Chemoreceptors Predicted to Stimulate the Che Pathway -- 7.3.5 The Che2 Pathway -- 7.3.6 Transcriptional and Post-transcriptional Regulation of Chemoreceptors and Chemosensory Pathways -- 7.4 Surface Sensing. 7.4.1 Modulation of c-di-GMP Levels by the Wsp Pathway -- 7.4.2 Twitching Motility and the Chp Pathway -- 7.4.3 The Role of the Wsp and Chp Pathways in Surface Sensing -- 7.4.4 Outlook -- References -- 8: Antimicrobial Weapons of Pseudomonas aeruginosa -- 8.1 Introduction -- 8.2 Contact-Dependent Antimicrobial Weapons -- 8.2.1 T5SS/CDI -- 8.2.1.1 Components and Mode of Action -- 8.2.1.2 Mechanisms of Prey Cell Targeting and Toxin Action -- 8.2.1.3 Role of CDI Weapons in Antimicrobial Competition -- 8.2.2 T6SS -- 8.2.2.1 Components and Mode of Action -- 8.2.2.2 Mechanism of Prey Cell Targeting and Toxin Action -- 8.2.2.3 Role of T6SS Weapons in Intermicrobial Competition -- 8.3 Contact-Independent Antimicrobial Weapons -- 8.3.1 Pyocins -- 8.3.1.1 R-and F-Type Tailocins -- 8.3.1.2 S-, L- and M-Type Pyocins -- 8.3.1.3 Pyocins as Epidemiological Markers -- 8.3.1.4 Role of Tailocins and Pyocins in Interbacterial Competition -- 8.3.1.5 Pyocins as Antibacterial Agents -- 8.3.2 Small Antimicrobial Molecules -- 8.3.2.1 Quorum Sensing Molecules as Antimicrobial Agents -- 8.3.2.2 Quorum Sensing-Regulated Production of Antimicrobial Agents -- 8.3.2.2.1 Staphylolytic Protease, LasA -- 8.3.2.2.2 Rhamnolipids -- 8.3.2.2.3 Hydrogen Cyanide -- 8.3.2.2.4 Phenazines -- 8.3.3 Siderophores Pyoverdine and Pyochelin -- 8.4 Membrane Vesicle-Packaged Antimicrobials -- 8.5 Conclusions and Future Directions -- References -- 9: Pseudomonas aeruginosa Antivirulence Strategies: Targeting the Type III Secretion System -- 9.1 Introduction -- 9.2 Small Molecule Inhibitors -- 9.2.1 ExoU Inhibitors -- 9.2.2 ExoS Inhibitors -- 9.3 Active Vaccines -- 9.3.1 PopB -- 9.3.2 PscC -- 9.3.3 PscF -- 9.3.4 PcrV -- 9.3.5 Killed Cells -- 9.4 Passive Antibody Approaches -- 9.5 Future Directions -- 9.6 Perspective -- References -- Part III: Pathogenesis and Virulence. 10: What Makes Pseudomonas aeruginosa a Pathogen?. |
| Record Nr. | UNINA-9910619277703321 |
| Cham, Switzerland : , : Springer, , [2022] | ||
| Materiale a stampa | ||
| Lo trovi qui: Univ. Federico II | ||
| ||