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Glycoinositolphospholipids from Trypanosoma cruzi interfere with macrophages and dendritic cell responses
Claudia Brodskyn1, Julie Patricio, Rubem Oliveira
1Centro de Pesquisa Gonçalo Moniz, FIOCRUZ, Instituto de Ciências da Saúde, Universidade Federal Bahia, Salvador, Brazil.
Insights
Trypanosoma cruzi glycoinositolphospholipid (GIPL) suppresses immune cells like macrophages and dendritic cells (DC). This immune modulation by GIPL may help the parasite evade the host immune response, contributing to disease pathogenesis.
Area of Science:
- Immunology
- Parasitology
- Cell Biology
Background:
- Antigen-presenting cells (APCs), including macrophages and dendritic cells (DCs), are crucial for initiating adaptive immune responses.
- Trypanosoma cruzi, the causative agent of Chagas disease, employs various strategies to evade host immunity.
- Glycoinositolphospholipids (GIPLs) are major surface molecules of Trypanosoma cruzi with potential immunomodulatory functions.
Purpose of the Study:
- To investigate the immunomodulatory effects of Trypanosoma cruzi GIPL on human macrophages and dendritic cells (DCs).
- To determine the impact of GIPL on the production of key cytokines and the expression of surface markers involved in immune activation.
Main Methods:
- Human macrophages and DCs were stimulated with lipopolysaccharide (LPS) in the presence or absence of T. cruzi GIPL.
- Cytokine levels (TNF-alpha, IL-8, IL-10, IL-12p40) in cell supernatants were measured using ELISA.
- Surface expression of immune markers (CD80, CD86, HLA-DR, CD40, CD57, CD83) was analyzed by flow cytometry.
Main Results:
- T. cruzi GIPL significantly decreased the secretion of TNF-alpha, IL-10, and IL-12p40 by both macrophages and DCs stimulated with LPS.
- GIPL down-regulated the expression of multiple surface molecules (CD80, CD86, HLA-DR, CD40, CD57) on macrophages and (HLA-DR, CD83, CD86, CD80, CD40) on DCs.
- The ceramide portion of GIPL was identified as the primary active component responsible for these immunomodulatory effects.
Conclusions:
- Trypanosoma cruzi GIPL exhibits potent immunosuppressive activities on human antigen-presenting cells.
- These immunoregulatory effects, particularly the inhibition of cytokine production and surface marker expression, likely contribute to parasite evasion of the host immune system.
- The findings suggest that T. cruzi GIPL plays a significant role in the pathogenesis of Chagas disease by dampening critical immune responses.
Abstract:
To investigate the possible effects of glycoinositolphospholipid (GIPL) from Trypanosoma cruzi on human antigen presenting cells, we tested their effects on lipopolysaccharide (LPS)-stimulated human macrophages and dendritic cells (DC). Human macrophages or DC were incubated with GIPL (50 microg/ml) and LPS (500 pg/ml) and tumor necrosis factor alpha (TNF-alpha), interleukin 8 (IL-8), IL-10, and IL-12p40 levels in supernatants were analyzed by enzyme-linked immunosorbent assay. TNF-alpha, IL-10, and IL-12 secretion were significantly decreased by GIPL both in macrophages and DC. In contrast, GIPL did not alter IL-8 production. We also analyzed the expression of CD80, CD86, HLA-DR, CD40, and CD57 on the macrophage surface after stimulation with LPS in the presence or absence of T. cruzi GIPL. GIPL led to a down-regulation in the expression of all tested molecules. We additionally examined the influence of T. cruzi GIPL on the response of human DC to LPS. LPS-induced HLA-DR, CD83, and CD86 up-regulation was significantly inhibited by GIPL. A slight down-regulation in CD80 and CD40 expression on DC surfaces in the presence of GIPL was also noticed. Similarly, GIPL led to down-modulation of CD83, CD80, CD86, and HLA-DR surface expression and TNF-alpha and IL-10 production when DC were stimulated by CD40L. The ceramide portion of GIPL was responsible for most of the activity exhibited by the whole molecule. Considering the important role of the immune response in determining the fate of the host-parasite relationship, the immunoregulatory activities of T. cruzi GIPL are potentially important for parasite evasion and then pathogenesis of infection with protozoan parasites.
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