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Isolation and Identification of Extravascular Immune Cells of the Heart
Published on: August 23, 2018
Do cardiomyocytes mount an immune response to Group A Streptococcus?
Zhi Li1, Amy E Bryant, Stephanie M Hamilton
1Infectious Diseases Section, Veterans Affairs Medical Center, Boise, ID 83702, USA. Zhi.Li@va.gov
Cytokine
|March 8, 2011
Summary
Group A Streptococcus can cause toxic shock syndrome (StrepTSS) leading to heart dysfunction. Cardiomyocyte-derived cytokines may explain this cardiac complication in StrepTSS patients.
Area of Science:
- Cardiovascular Medicine
- Infectious Diseases
- Immunology
Background:
- Group A Streptococcal toxic shock syndrome (StrepTSS) is associated with a distinct cardiomyopathy.
- This cardiomyopathy presents with global hypokinesia and reduced cardiac index.
Purpose of the Study:
- To investigate the immune response of cardiomyocytes to Group A Streptococcus (GAS).
- To explore the role of cardiomyocyte-derived cytokines in StrepTSS-associated cardiomyopathy.
Main Methods:
- In vivo and in vitro studies were conducted.
- Cardiomyocyte immune responses to direct GAS stimulation and GAS-activated inflammatory cells were analyzed.
Main Results:
- Cardiomyocytes produce cytokines upon direct GAS stimulation.
- Cytokines are also produced following exposure to GAS-activated inflammatory cells.
- Cardiomyocyte-derived cytokines were identified following GAS exposure.
Conclusions:
- Locally produced, cardiomyocyte-derived cytokines may mediate cardiac contractile dysfunction in StrepTSS.
- These cytokines represent a potential therapeutic target for mitigating StrepTSS-associated cardiomyopathy.
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