2 options
The human microbiota and chronic disease : dysbioses as a cause of human pathology / edited by Brian Henderson and Luigi Nibali.
- Format:
- Book
- Language:
- English
- Subjects (All):
- Human body--Microbiology.
- Human body.
- Chronic diseases.
- Physical Description:
- 1 online resource (563 p.)
- Edition:
- 1st ed.
- Place of Publication:
- Hoboken, New Jersey : Wiley-Blackwell, 2016.
- Language Note:
- English
- Summary:
- Microbiota-associated pathology can be a direct result of changes in general bacterial composition, such as might be found in periodontitis and bacterial vaginosis, and/or as the result of colonization and/or overgrowth of so called keystone species. The disruption in the composition of the normal human microbiota, or dysbiosis, plays an integral role in human health and human disease. The Human Microbiota and Human Chronic Disease: Dysbioses as a Cause of Human Pathology discusses the role of the microbiota in maintaining human health. The text introduces the reader to the biology of microbial dysbiosis and its potential role in both bacterial disease and in idiopathic chronic disease states. Divided into five sections, the text delineates the concept of the human bacterial microbiota with particular attention being paid to the microbiotae of the gut, oral cavity and skin. A key methodology for exploring the microbiota, metagenomics, is also described. The book then shows the reader the cellular, molecular and genetic complexities of the bacterial microbiota, its myriad connections with the host and how these can maintain tissue homeostasis. Chapters then consider the role of dysbioses in human disease states, dealing with two of the commonest bacterial diseases of humanity - periodontitis and bacterial vaginosis. The composition of some, if not all microbiotas can be controlled by the diet and this is also dealt with in this section. The discussion moves on to the major 'idiopathic' diseases afflicting humans, and the potential role that dysbiosis could play in their induction and chronicity. The book then concludes with the therapeutic potential of manipulating the microbiota, introducing the concepts of probiotics, prebiotics and the administration of healthy human faeces (faecal microbiota transplantation), and then hypothesizes as to the future of medical treatment viewed from a microbiota-centric position. * Provides an introduction to dysbiosis, or a disruption in the composition of the normal human microbiota * Explains how microbiota-associated pathology and other chronic diseases can result from changes in general bacterial composition * Explores the relationship humans have with their microbiota, and its significance in human health and disease * Covers host genetic variants and their role in the composition of human microbial biofilms, integral to the relationship between human health and human disease Authored and edited by leaders in the field, The Human Microbiota and Human Chronic Disease will be an invaluable resource for clinicians, pathologists, immunologists, cell and molecular biologists, biochemists, and system biologists studying cellular and molecular bases of human diseases.
- Contents:
- Intro
- Title Page
- Copyright Page
- Contents
- List of contributors
- Preface
- SECTION 1 An introduction to the human tissue microbiome
- Chapter 1 The human microbiota: an historical perspective
- 1.1 Introduction: the discovery of the human microbiota: why do we care?
- 1.2 The importance of the indigenous microbiota in health and disease
- 1.2.1 The indigenous microbiota and human disease
- 1.2.2 The indigenous microbiota and human health
- 1.3 The development of technologies for characterising the indigenous microbiota
- 1.3.1 Light microscopy
- 1.3.2 Electron microscopy
- 1.3.3 Culture-based approaches to microbial community analysis
- 1.4 Culture-independent approaches to microbial community analysis
- 1.5 Determination of microbial community functions
- 1.6 Closing remarks
- Take-home message
- References
- Chapter 2 An introduction to microbial dysbiosis
- 2.1 Definition of dysbiosis
- 2.2 The 'normal' microbiota
- 2.3 Main features of dysbiosis
- 2.4 Conclusions
- Acknowledgment
- Chapter 3 The gut microbiota: an integrated interactive system
- 3.1 Introduction
- 3.2 Who is there, how is it composed?
- 3.3 A system in interaction with food
- 3.4 A system highly impacted by the host
- 3.5 A system in interaction with human cells
- 3.6 Conclusion: an intriguing integrated interactive system deserving further study
- Chapter 4 The oral microbiota
- 4.1 Introduction
- 4.2 Composition of the oral microbiome
- 4.2.1 Archaea
- 4.2.2 Fungi
- 4.2.3 Protozoa
- 4.2.4 Viruses
- 4.2.5 Bacteria
- 4.3 The oral microbiota in health
- 4.3.1 Evolution of the oral microbiota
- 4.3.2 Role of oral bacteria in health
- 4.4 Role of oral microbiome in disease
- 4.4.1 Dental caries
- 4.4.2 Gingivitis
- 4.4.3 Oral bacteria and non‐oral disease.
- 4.5 Future outlook
- Chapter 5 The skin microbiota
- 5.1 Normal skin
- 5.2 Skin diseases
- 5.2.1 Atopic dermatitis
- 5.2.2 Psoriasis
- 5.2.3 Acne
- 5.2.4 Rosacea
- 5.2.5 Seborrheic dermatitis and dandruff
- 5.2.6 Primary immunodeficiencies
- 5.3 Experimental studies
- 5.4 Dynamics of the skin microbiome
- 5.5 Axillary skin microbiome transplantation
- 5.6 Mouse skin microbiome studies
- 5.7 Concluding remarks
- Chapter 6 Metagenomic analysis of the human microbiome
- 6.1 Introduction
- 6.2 The human microbiome
- 6.3 Changes in microbiota composition during host life cycles
- 6.4 The human microbiome and the environment
- 6.5 Disease and health implications of microbiome
- 6.5.1 The skin microbiota
- 6.5.2 The airway microbiome
- 6.5.3 Vaginal microbiome
- 6.5.4 Gut microbiota and disease
- 6.5.5 Metabolic disorders (obesity/diabetes)
- 6.6 Conclusions
- SECTION 2 Microbiota-microbiota and microbiota-host interactions in health and disease
- Chapter 7 Systems biology of bacteria‐host interactions
- 7.1 Introduction
- 7.2 Computational analysis of host‐microbe interactions
- 7.2.1 Analysis of metagenomic data
- 7.2.2 Metabolic reconstruction through comparative genomics
- 7.3 Network-based modeling
- 7.3.1 Topological network modeling
- 7.3.2 Constraint-based modeling
- 7.3.3 Metabolic reconstructions of human metabolism
- 7.3.4 Constraint-based modeling of host-microbe interactions
- 7.4 Other computational modeling approaches
- 7.4.1 Ordinary differential equation (ODE) models
- 7.4.2 Kinetic modeling
- 7.5 Conclusion
- Acknowledgments
- Chapter 8 Bacterial biofilm formation and immune evasion mechanisms
- 8.1 Introduction
- 8.2 Biofilms in human disease.
- 8.3 Biofilm formation
- 8.4 Immune responses to biofilms
- 8.4.1 Innate immune responses
- 8.4.2 Adaptive immune responses
- 8.4.3 Fibroblasts, epithelial cells and other immune responses
- 8.5 Biofilm immune evasion strategies
- 8.6 Vaccines and biofilm therapeutics
- 8.7 Conclusions
- Take-Home Message
- Chapter 9 Co-evolution of microbes and immunity and its consequences for modern-day life
- 9.1 Introduction
- 9.2 Symbiosis in eukaryotic evolution
- 9.3 Evolution of the (innate and adaptive) immune system
- 9.3.1 Immune proteins
- 9.3.2 Evolution of adaptive immunity
- 9.3.3 Two separate adaptive immune systems evolved
- 9.4 Hygiene hypothesis
- 9.5 What drives the composition of the microbiota?
- 9.6 The pace of evolution
- Chapter 10 How viruses and bacteria have shaped the human genome: the implications for disease
- 10.1 Genetic symbiosis
- 10.2 Mitochondria: symbiogenesis in the human
- 10.3 Viral symbiogenesis
- 10.4 HERV proteins
- Chapter 11 The microbiota as an epigenetic control mechanism
- 11.1 Introduction
- 11.2 Background on epigenetics and epigenomic programming/reprograming
- 11.3 Epigenomics and link with energy metabolism
- 11.4 The microbiota as a potential epigenetic modifier
- 11.5 Epigenetic control of the host genes by pathogenic and opportunistic microorganisms
- 11.6 Epigenetic control of the host genes by indigenous (probiotic) microorganisms
- 11.7 Concluding remarks and future directions
- Chapter 12 The emerging role of propionibacteria in human health and disease
- 12.1 Introduction
- 12.2 Microbiological features of propionibacteria
- 12.3 Population structure of P. acnes
- 12.4 Propionibacteria as indigenous probiotics of the skin.
- 12.5 Propionibacteria as opportunistic pathogens
- 12.6 Host interacting traits and factors of propionibacteria
- 12.7 Host responses to P. acnes
- 12.7.1 Innate immune responses
- 12.7.2 Adaptive immune responses
- 12.7.3 Host cell tropism of P. acnes
- 12.8 Propionibacterium-specific bacteriophages
- 12.9 Concluding remarks
- SECTION 3 Dysbioses and bacterial diseases: Metchnikoff's legacy
- Chapter 13 The periodontal diseases: microbial diseases or diseases of the host response?
- 13.1 The tooth: a potential breach in the mucosal barrier
- 13.2 The periodontium from health to disease
- 13.3 Periodontitis: one of the most common human diseases
- 13.4 Periodontal treatment: a non‐specific biofilm disruption
- 13.5 Microbial etiology
- 13.6 The host response in periodontitis
- 13.7 Conclusions
- Chapter 14 The polymicrobial synergy and dysbiosis model of periodontal disease pathogenesis
- 14.1 Introduction
- 14.2 A (very) polymicrobial etiology of periodontitis
- 14.3 Synergism among periodontal bacteria
- 14.4 Interactions between bacterial communities and epithelial cells
- 14.5 Manipulation of host immunity
- 14.6 Conclusions
- Chapter 15 New paradigm in the relationship between periodontal disease and systemic diseases: effects of oral bacteria on the gut microbiota and metabolism
- 15.1 Introduction
- 15.2 Association between periodontal and systemic diseases
- 15.2.1 Periodontal disease and diabetes
- 15.2.2 Periodontal disease and atherosclerotic vascular diseases
- 15.2.3 Periodontal disease and rheumatoid arthritis
- 15.2.4 Periodontal disease and non‐alcoholic fatty liver disease
- 15.2.5 Periodontal disease and pre‐term birth
- 15.2.6 Periodontal disease and obesity.
- 15.2.7 Periodontal disease and cancer
- 15.2.8 Periodontal disease and inflammatory bowel disease
- 15.3 Issues in causal mechanisms of periodontal disease for systemic disease
- 15.3.1 Endotoxemia (bacteremia)
- 15.3.2 Inflammatory mediators
- 15.3.3 Autoimmune response from molecular mimicry
- 15.4 New insights into the mechanisms linking periodontal disease and systemic disease
- 15.5 Effect of oral administration of P. gingivalis on metabolic change and gut microbiota
- 15.6 Conclusions
- Chapter 16 The vaginal microbiota in health and disease
- 16.1 What makes a healthy microbiota
- 16.1.1 How does the vaginal microbiota mediate healthiness?
- 16.1.2 Establishment of the vaginal microbiota
- 16.1.3 The role of host genetic variation on vaginal health
- 16.1.4 Impact of age, menstrual cycle and environmental factors on vaginal health
- 16.2 The vaginal microbiota in disease
- 16.2.1 Bacterial vaginosis
- 16.2.2 Clinical consequences of altered vaginal microbiota (see Figure 1)
- 16.2.3 Vaginal microbiota and transmission and susceptibility to HIV infection
- 16.3 Conclusions
- SECTION 4 Dysbioses and chronic diseases: is there a connection?
- Chapter 17 Reactive arthritis: the hidden bacterial connection
- 17.1 Introduction
- 17.2 Reactive arthritis
- 17.3 Pathophysiology of ReA
- 17.4 Questions remain
- 17.5 Conclusion
- Chapter 18 Rheumatoid arthritis: the bacterial connection
- 18.1 Preclinical rheumatoid arthritis
- 18.2 Predisposition to RA
- 18.3 MCH-HLA and genetic predisposition to RA
- 18.4 Molecular mimicry in RA
- 18.5 Innate immune system and RA
- 18.6 Bystander activation and pattern recognition receptors
- 18.7 Antibodies and neoepitopes
- 18.8 Superantigens
- 18.9 LPS.
- 18.10 Bacterial DNA and peptidoglycans.
- Notes:
- Description based upon print version of record.
- Includes bibliographical references at the end of each chapters and index.
- Description based on print version record.
- ISBN:
- 9781118982891
- 1118982894
- 9781118982884
- 1118982886
- 9781118982907
- 1118982908
- OCLC:
- 950902016
The Penn Libraries is committed to describing library materials using current, accurate, and responsible language. If you discover outdated or inaccurate language, please fill out this feedback form to report it and suggest alternative language.