Experimental evidences that P21 protein controls Trypanosoma cruzi replication and modulates the pathogenesis of

Thaise L Teixeira1, Patrícia Castilhos1, Cassiano C Rodrigues1

  • 1Laboratório de Tripanosomatídeos, Departamento de Imunologia, Instituto de Ciências Biomédicas, Universidade Federal de Uberlândia, Rua Piauí, Bloco 2B Sala 200 Campus Umuarama, 38400-902, Uberlândia, MG, Brazil.

Insights

The Trypanosoma cruzi (T. cruzi) protein P21, when administered as recombinant P21 (rP21), reduced parasite load and cardiac fibrosis in infected mice. P21 also inhibited parasite growth and replication, suggesting a role in host-parasite survival.

Area of Science:

  • Parasitology
  • Immunology
  • Molecular Biology

Background:

  • P21 is a Trypanosoma cruzi (T. cruzi) secreted protein with known roles in phagocytosis, leukocyte chemotaxis, and angiogenesis inhibition.
  • The specific function of P21 during active T. cruzi infection has not been previously elucidated.

Purpose of the Study:

  • To investigate the role and therapeutic potential of P21 in a murine model of late-stage T. cruzi infection.

Main Methods:

  • Treatment of infected mice with recombinant P21 (rP21).
  • Assessment of parasite load, cardiac tissue fibrosis, and angiogenesis.
  • In vitro evaluation of rP21 effects on T. cruzi epimastigote growth and amastigote replication.
  • Analysis of parasite cell cycle modulation by rP21.

Main Results:

  • rP21 treatment significantly reduced parasite burden in infected mice.
  • Cardiac angiogenesis was decreased, while fibrosis was induced by rP21.
  • rP21 inhibited the in vitro growth of epimastigotes and intracellular replication of amastigotes.
  • rP21 modulated the cell cycle of T. cruzi parasites.

Conclusions:

  • P21 plays a crucial role in controlling T. cruzi replication within the host.
  • rP21 demonstrates therapeutic potential for Chagas disease by reducing parasite load and modulating host tissue response.
  • P21 appears to support the survival of both the parasite and the host during infection.

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