Chagas Disease

Contributors of Volume 76

Preface

Bioactive Lipids in Trypanosoma cruzi Infection

Abbreviations

1.1. Introduction

1.2. Eicosanoid Synthesis in Vertebrates

1.3. Lipid Metabolism and Eicosanoid Biosynthetic Pathways in Trypanosoma cruzi

1.4. Endogenous Regulation of Eicosanoids During Experimental Chagas Disease

1.5. Lessons from Pharmacological Manipulation and from Null Mice

Acknowledgements

Mechanisms of Host Cell Invasion by Trypanosoma cruzi

2.1. Introduction

2.2. General Features of Trypanosoma cruzi Invasion

2.3. To the Lysosome … and Beyond

2.4. Disruption of the Parasitophorous Vacuole Membrane and Cytosolic Localization of Parasites

2.5. The Role of the Host Cell Cytoskeleton in Trypanosoma cruzi Trypomastigote Invasion of Non-Phagocytic Cells

2.6. The Discovery of Reversible Invasion

2.7. Concluding Remarks

Gap Junctions and Chagas Disease

3.1. Introduction

3.2. Loss of Gap Junctions and Coupling in Rodent Chagasic Cardiomyopathy

3.3. Not All Junctional Proteins are Affected by Trypanosoma cruzi Infection

3.4. Microarray Experiments have Revealed Profound Changes in Gene Expression in the Chagasic Mouse, Both in Acute and in Chronic Disease Phases

3.5. Conclusions

The Vasculature in Chagas Disease

4.1. Historical Aspects

4.2. Small Animal Studies of the Microcirculation in Trypanosoma cruzi Infection

4.3. Studies in Dogs

4.4. Vasoactive Peptides and Eicosanoids

4.5. In Vitro Studies

4.6. Studies in Humans

4.7. Conclusions

Acknowledgements

Infection-Associated Vasculopathy in Experimental Chagas Disease

Abbreviations

5.1. Introduction

5.2. A Brief Overview on the Immunopathogenesis of Chagas Disease

5.3. Future Directions

Acknowledgements

Autoimmunity

6.1. Introduction

6.2. Natural History of Chagas Disease

6.3. Heart-Specific Inflammatory Lesions in CCC: Parasite Antigen-Driven Immunopathology?

6.4. Immunopathogenesis of CCC

6.5. Autoimmunity in Chagas Disease

6.6. Molecular Mimicry

6.7. Conclusion

ROS Signalling of Inflammatory Cytokines During Trypanosoma cruzi Infection

7.1. Reactive Oxygen Species and Source

7.2. Inflammatory Cytokines During Trypanosoma cruzi Infection and Chagas Disease

7.3. ROS Signalling of Cytokine Responses

7.4. The Impact of Oxidative Stress and Cytokine Mediators and Cardiac Dysfunction

7.5. Conclusions and Future Directions

Acknowledgements

Inflammation and Chagas Disease

8.1. The Multiple Roles of Inflammation in Chagas Disease

8.2. Experimental Models for Studying Inflammation and Immune Mechanisms in Chagas Disease

8.3. Mediators of Protection in Experimental Trypanosoma cruzi Infection

8.4. Mediators of Inflammation and Their Role in Mediating Tissue Damage and Protection in Experimental Trypanosoma cruzi Infection

8.5. Conclusion

Acknowledgements

Neurodegeneration and Neuroregeneration in Chagas Disease

9.1. Introduction

9.2. Involvement of the Autonomic Nervous System in CD Pathogenesis

9.3. Mechanism of Neuronal Damage

9.4. Neuroregeneration

9.5. Trans-Sialidase/Parasite-Derived Neurotrophic Factor

9.6. Conclusions

Adipose Tissue, Diabetes and Chagas Disease

10.1. Introduction

10.2. Adiponectin

10.3. Adipose Tissue and Infection

10.4. Chagas Disease and Adipose Tissue

10.5. Chagas Disease and Glycaemia

10.6. Conclusions

Acknowledgements