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.

Infection and Immunity
|April 22, 2020
PubMed

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.

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