Protein deficiency alters CX3CL1 and endothelin-1 in experimental Trypanosoma cruzi-induced cardiomyopathy

Régia F Martins1, Patrícia M Martinelli, Paulo M M Guedes

  • 1Núcleo de Pesquisas em Ciências Biológicas, Universidade Federal de Ouro Preto, Ouro Preto, Brazil.

Insights

Protein malnutrition exacerbates Chagas heart disease by increasing endothelin-1 and CX3CL1 levels. This nutritional deficiency impairs the host

Area of Science:

  • Immunology
  • Nutritional Science
  • Parasitology

Background:

  • Chagas heart disease, a complication of Trypanosoma cruzi infection, is influenced by host nutritional status.
  • Protein malnutrition can lead to secondary immunodeficiency, potentially worsening parasitic infections.
  • Endothelin-1 and CX3CL1 are implicated in inflammatory processes.

Purpose of the Study:

  • To investigate the impact of a low protein diet on endothelin-1 and CX3CL1 production in a Trypanosoma cruzi infection model.
  • To assess the role of nutritional status in modulating inflammatory mediators during Chagas disease.

Main Methods:

  • Fisher rats were fed either a low protein (6%) or normal protein (15%) diet.
  • Animals were infected with the Y strain of Trypanosoma cruzi.
  • Parasitemia, immune cell infiltration (including macrophage phenotypes), and levels of endothelin-1 and CX3CL1 were evaluated at acute and chronic phases.

Main Results:

  • Low protein diet reduced body weight and serum proteins but elevated circulating CX3CL1 and endothelin-1 in infected rats.
  • Infected rats on a low protein diet showed uncontrolled parasitemia.
  • Cardiac tissue in the acute phase exhibited reduced CX3CL1, endothelin-1, and leukocyte infiltration, particularly CD68 and CD163 macrophages, in the low protein group.

Conclusions:

  • Endothelin-1 and CX3CL1 play a role in the inflammatory response during Chagas disease.
  • Host nutritional status, specifically protein intake, can modulate the levels of these inflammatory mediators.
  • Dietary protein influences the control of parasitemia and cardiac inflammation in experimental Chagas disease.
Abstract

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