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Modulation of chagasic cardiomyopathy by interleukin-4: dissociation between inflammation and tissue parasitism
M B Soares1, K N Silva-Mota, R S Lima
1Gonçalo Moniz Research Center - Fundaçào Oswaldo Cruz, Rua Waldemar Falcão, 121-Brotas-Salvador, Bahia, Brazil 40295-001.
Insights
Interleukin-4-deficient mice show reduced Trypanosoma cruzi parasite load and mortality but increased heart inflammation. This suggests a complex balance between T helper cell responses in chronic chagasic cardiomyopathy.
Area of Science:
- Immunology
- Cardiology
- Infectious Diseases
Background:
- Chronic chagasic cardiomyopathy (CChC) involves inflammation leading to heart damage.
- Trypanosoma cruzi infection triggers immune responses that influence disease progression.
Purpose of the Study:
- To investigate the role of interleukin-4 (IL-4) in the immune response to Trypanosoma cruzi infection.
- To determine the impact of IL-4 deficiency on cardiac inflammation, parasitism, and mortality in a mouse model of CChC.
Main Methods:
- Utilized interleukin-4-deficient mice and wild-type mice infected with Trypanosoma cruzi.
- Assessed T helper (Th) 1 immune responses, parasite load, cardiac inflammation, and mortality.
Main Results:
- IL-4-deficient mice exhibited heightened Th1 responses compared to wild-type controls.
- These mice displayed reduced parasite burdens and lower mortality rates.
- A significant exacerbation of cardiac inflammation was observed in IL-4-deficient mice, dissociating inflammation from parasite load.
Conclusions:
- A delicate balance between Th responses is crucial in CChC.
- While Th1 responses can control Trypanosoma cruzi parasitism, they may also enhance cardiac inflammation.
- Modulating Th responses could be key to managing host and parasite survival in Chagas disease.
Abstract:
Chronic chagasic cardiomyopathy (CChC) is characterized by an inflammatory reaction which may eventually lead to heart enlargement, arrythmia, and death. As described herein, interleukin-4-deficient mice mount increased specific T helper (Th) 1 immune responses when infected with Trypanosoma cruzi, as compared to wild-type mice. Interestingly, these mice had reduced parasitism and mortality and exacerbated inflammation in their hearts, demonstrating a clear dissociation between inflammation and parasite load. The modulation of these phenomena so as to maximize host and parasite survivals may depend on a fine balance between Th responses, in which a Th1 response will, on one hand, control parasitism and, on the other hand, enhance heart inflammation throughout the course of the infection.