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Parasite Induced Genetically Driven Autoimmune Chagas Heart Disease in the Chicken Model
Published on: July 29, 2012
Pathogenesis of Chagas heart disease: role of autoimmunity
1Departments of Pathology and Microbiology-Immunology, and Feinberg Cardiovascular Research Institute, Northwestern University Medical School, Chicago, IL 60611, USA. d-engman@northwestern.edu
Insights
Chagas heart disease, caused by Trypanosoma cruzi, may have an autoimmune component. New evidence supports autoimmunity contributing to cardiac inflammation alongside other mechanisms in this parasitic infection.
Area of Science:
- Immunology
- Infectious Diseases
- Cardiology
Background:
- Chagas heart disease results from Trypanosoma cruzi infection.
- The lack of detectable parasites in affected hearts suggests non-parasitic causes like autoimmunity.
- Testing the autoimmunity hypothesis is challenging due to coexisting inflammation mechanisms.
Purpose of the Study:
- To review proposed Chagas disease pathogenesis mechanisms.
- To present new evidence supporting an autoimmune contribution to cardiac inflammation.
- To offer fresh perspectives on the Chagas disease autoimmunity debate.
Main Methods:
- Literature review of Chagas disease pathogenesis.
- Analysis of existing evidence regarding autoimmune contributions.
- Synthesis of current understanding and new data.
Main Results:
- Multiple mechanisms contribute to Chagas disease pathogenesis.
- Evidence suggests an autoimmune component plays a role in cardiac inflammation.
- The precise role of autoimmunity remains under investigation.
Conclusions:
- Autoimmunity is a plausible contributing factor to Chagas heart disease.
- Further research is needed to definitively establish the role of autoimmunity.
- Understanding all pathogenic mechanisms is crucial for effective treatment.
Abstract:
Chagas heart disease is caused by infection with the protozoan parasite Trypanosoma cruzi. The apparent absence of parasites from the hearts of most individuals who succumb to this illness has led some to propose an autoimmune basis for disease pathogenesis. This hypothesis has been extremely difficult to test, because other mechanisms of tissue inflammation may coexist in the setting of active infection. Here we review the proposed mechanisms of Chagas disease pathogenesis and present new evidence in support of an autoimmune contribution to cardiac inflammation in the context of these other mechanisms. While we do not yet have a definitive answer to the autoimmunity question, we hope that our views will provide those engaged in the debate fresh perspective on this challenging issue.
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