Related Experiment Video

Updated: Jun 30, 2026

Establishment of Larval Zebrafish as an Animal Model to Investigate Trypanosoma cruzi Motility In Vivo
13:21

Establishment of Larval Zebrafish as an Animal Model to Investigate Trypanosoma cruzi Motility In Vivo

Published on: September 30, 2017

11.1K

Interaction of Signaling Lymphocytic Activation Molecule Family 1 (SLAMF1) receptor with Trypanosoma cruzi is

Cristina Poveda1, Alfonso Herreros-Cabello1, Francisco Callejas-Hernández1

  • 1Centro de Biología Molecular Severo Ochoa, Consejo Superior de Investigaciones Científicas, Universidad Autónoma de Madrid, Cantoblanco, Madrid, Spain.

Plos Neglected Tropical Diseases
|September 14, 2020
PubMed

Insights

Signaling Lymphocyte-Activation Molecule Family 1 (SLAMF1) influences susceptibility to Trypanosoma cruzi infections. Parasite strain diversity impacts SLAMF1

Area of Science:

  • Immunology
  • Parasitology
  • Molecular Biology

Background:

  • Signaling Lymphocyte-Activation Molecule Family 1 (SLAMF1) is implicated in host susceptibility to Trypanosoma cruzi infection.
  • The role of parasite genetic diversity in modulating SLAMF1-mediated disease susceptibility remains unclear.

Purpose of the Study:

  • To investigate the influence of Trypanosoma cruzi strain diversity on SLAMF1's role in infection susceptibility.
  • To elucidate the mechanisms by which SLAMF1 affects parasite load, immune cell activation, and host survival.

Main Methods:

  • Interaction of SLAMF1 with T. cruzi strains was confirmed using fluorescence microscopy, flow cytometry, and qPCR.
  • Parasite load, NADPH oxidase (NOX2) expression, and reactive oxygen species (ROS) production were assessed in SLAMF1-deficient (Slamf1-/-) and wild-type (BALB/c) macrophages.
  • In vivo studies evaluated host immune responses and survival in mice infected with different T. cruzi strains.

Main Results:

  • Most T. cruzi strains showed reduced parasite load in Slamf1-/- macrophages, accompanied by increased NOX2 expression and ROS production.
  • The VFRA strain exhibited distinct behavior, with higher parasite load and lower NOX2/ROS in Slamf1-/- macrophages.
  • In vivo, SLAMF1 deficiency protected mice against lethal Y strain infection by promoting a proinflammatory response.

Conclusions:

  • Trypanosoma cruzi strain-dependent interactions with SLAMF1 modulate ROS production, parasite replication in macrophages, and host survival.
  • SLAMF1 plays a critical role in controlling T. cruzi infection, with its impact varying based on parasite genetic diversity.
  • Further research is needed to identify parasite molecules involved in SLAMF1 interaction to fully understand disease immunopathogenesis.

More Related Videos

Introducing a Gene Knockout Directly Into the Amastigote Stage of Trypanosoma cruzi Using the CRISPR/Cas9 System06:13

Introducing a Gene Knockout Directly Into the Amastigote Stage of Trypanosoma cruzi Using the CRISPR/Cas9 System

Published on: July 31, 2019

9.4K
Quantitative 3D Imaging of Trypanosoma cruzi-Infected Cells, Dormant Amastigotes, and T Cells in Intact Clarified Organs08:17

Quantitative 3D Imaging of Trypanosoma cruzi-Infected Cells, Dormant Amastigotes, and T Cells in Intact Clarified Organs

Published on: June 23, 2022

3.5K

Related Concept Videos

American Trypanosomiasis01:22

American Trypanosomiasis

Chagas disease, or American trypanosomiasis, is a vector-borne parasitic infection caused by Trypanosoma cruzi, a flagellated protozoan (kinetoplastid) of the family Trypanosomatidae. The disease is endemic in Latin America, although cases are increasingly reported worldwide due to human migration. Transmission most commonly occurs when feces of infected triatomine bugs contaminate bite wounds or mucosal surfaces; additional routes include congenital, transfusional, transplant-related, and oral...
Antiprotozoal Agents01:21

Antiprotozoal Agents

Leishmaniasis is a widespread parasitic disease caused by several Leishmania species. It affects millions of people each year and remains a major public health problem in endemic regions. First-line treatment relies on pentavalent antimonials, including meglumine antimoniate and sodium stibogluconate. Even so, how these drugs work has not been fully clear, especially their interaction with parasite-specific biochemical pathways. One key target is trypanothione reductase (TR), an enzyme that...