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Updated: Dec 23, 2025
Ultrastructural Expansion Microscopy in Three In Vitro Life Cycle Stages of Trypanosoma cruzi
Published on: May 12, 2023
MicroRNA-155 Deficiency Exacerbates Trypanosoma cruzi Infection
Bijay K Jha1, Sanjay Varikuti2, Gabriella R Seidler2
1Division of Infectious Diseases, Department of Internal Medicine, The Ohio State University Wexner Medical Center, Columbus, Ohio, USA.
Abstract:
Chagas disease, caused by the intracellular protozoan parasite Trypanosoma cruzi, is a public health problem affecting 6 to 8 million people, mainly in Latin America. The role of microRNAs in the pathogenesis of Chagas disease has not been well described. Here, we investigate the role of microRNA-155 (miR-155), a proinflammatory host innate immune regulator responsible for T helper type 1 and type 17 (Th1 and Th17) development and macrophage responses during T. cruzi infection. For this, we compared the survival and parasite growth and distribution in miR-155-/- and wild-type (WT) C57BL/6 mice. The lack of miR-155 caused robust parasite infection and diminished survival of infected mice, while WT mice were resistant to infection. Immunological analysis of infected mice indicated that, in the absence of miR-155, there was decreased interferon gamma (IFN-γ) and tumor necrosis factor alpha (TNF-α) production. In addition, we found that there was a significant reduction of CD8-positive (CD8+) T cells, natural killer (NK) cells, and NK-T cells and increased accumulation of neutrophils and inflammatory monocytes in miR-155-/- mice. Collectively, these data indicate that miR-155 is an important immune regulatory molecule critical for the control of T. cruzi infection.
Insights
MicroRNA-155 (miR-155) is crucial for controlling Trypanosoma cruzi infection. Its absence leads to increased parasite load and reduced survival in mice, highlighting its role in host defense against Chagas disease.
Area of Science:
- Immunology
- Parasitology
- Molecular Biology
Background:
- Chagas disease, caused by Trypanosoma cruzi, affects millions globally.
- The role of microRNAs in Chagas disease pathogenesis is poorly understood.
- MicroRNA-155 (miR-155) is a key regulator of the innate immune response.
Purpose of the Study:
- To investigate the role of miR-155 in the host immune response to Trypanosoma cruzi infection.
- To determine the impact of miR-155 deficiency on parasite control and host survival.
Main Methods:
- Comparison of survival, parasite load, and immune cell populations in miR-155 knockout (miR-155-/-) and wild-type (WT) mice infected with T. cruzi.
- Analysis of cytokine production (IFN-γ, TNF-α) and immune cell subsets (CD8+ T cells, NK cells, neutrophils, monocytes).
Main Results:
- miR-155-/- mice exhibited significantly reduced survival and increased parasite burden compared to WT mice.
- Absence of miR-155 led to decreased production of IFN-γ and TNF-α.
- miR-155 deficiency resulted in reduced CD8+ T cells, NK cells, and NK-T cells, with increased neutrophils and inflammatory monocytes.
Conclusions:
- miR-155 is essential for effective control of Trypanosoma cruzi infection.
- miR-155 plays a critical role in regulating the adaptive and innate immune responses necessary for combating Chagas disease.
