Fibrogenesis and collagen resorption in the heart and skeletal muscle of Calomys callosus experimentally infected with Trypanosoma cruzi: immunohistochemical identification of extracellular matrix components

Magalhães-Santos, Isis Fernandes; Lima, Elianita Suzart; Andrade, Sônia Gumes

doi:10.1590/s0074-02762002000500021

Cited by 8 publications

(1 citation statement)

References 18 publications

(14 reference statements)

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“…It was suggested that the gp85/trans-sialidase interacts with the ECM components (Alves and Colli, 2008) and speculated that the prolyl oligopeptidase Tc 80 may be involved in the infection possibly by acting on ECM components (Grellier et al, 2001). Interestingly, it was found that in a T. cruzi infected mouse embryo hepatocyte cell line, there was a reduction of MMP9 (Nogueira de Melo et al, 2004), as well as some matrix components during the late phase of infection (60th to 90th day; Magalhaes-Santos et al, 2002). Pinho et al (2002) reported that uncharacterized parasite antigens bind to non-infected cells and that ECM components were recognized by antibodies, however the molecular characterization of antigens and the specificity of these possible interactions were not considered.…”

Section: Some Potential Implications Of the Ecm In Infectionmentioning

confidence: 99%

Regulation and use of the extracellular matrix by Trypanosoma cruzi during early infection

Nde¹,

Lima²,

Johnson³

et al. 2012

Front. Immun.

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Chagas disease, which was once thought to be confined to endemic regions of Latin America, has now gone global becoming a new worldwide challenge. For more than a century since its discovery, it has remained neglected with no effective drugs or vaccines. The mechanisms by which Trypanosoma cruzi regulates and uses the extracellular matrix (ECM) to invade cells and cause disease are just beginning to be understood. Here we critically review and discuss the regulation of the ECM interactome by T. cruzi, the use of the ECM by T. cruzi and analyze the molecular ECM/T. cruzi interphase during the early process of infection. It has been shown that invasive trypomastigote forms of T. cruzi use and modulate components of the ECM during the initial process of infection. Infective trypomastigotes up-regulate the expression of laminin γ-1 (LAMC1) and thrombospondin (THBS1) to facilitate the recruitment of trypomastigotes to enhance cellular infection. Silencing the expression of LAMC1 and THBS1 by stable RNAi dramatically reduces trypanosome infection. T. cruzi gp83, a ligand that mediates the attachment of trypanosomes to cells to initiate infection, up-regulates LAMC1 expression to enhance cellular infection. Infective trypomastigotes use Tc85 to interact with laminin, p45 mucin to interact with LAMC1 through galectin-3 (LGALS3), a human lectin, and calreticulin (TcCRT) to interact with TSB1 to enhance cellular infection. Silencing the expression of LGALS3 also reduces cellular infection. Despite the role of the ECM in T. cruzi infection, almost nothing is known about the ECM interactome networks operating in the process of T. cruzi infection and its ligands. Here, we present the first elucidation of the human ECM interactome network regulated by T. cruzi and its gp83 ligand that facilitates cellular infection. The elucidation of the human ECM interactome regulated by T. cruzi and the dissection of the molecular ECM/T. cruzi interphase using systems biology approaches are not only critically important for the understanding of the molecular pathogenesis of T. cruzi infection but also for developing novel approaches of intervention in Chagas disease.

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Section: Some Potential Implications Of the Ecm In Infectionmentioning

confidence: 99%

Regulation and use of the extracellular matrix by Trypanosoma cruzi during early infection

Nde¹,

Lima²,

Johnson³

et al. 2012

Front. Immun.

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Trypanosoma cruzi–cardiomyocyte interaction: role of fibronectin in the recognition process and extracellular matrix expression in vitro and in vivo

Calvet

Meuser

Almeida

et al. 2004

Experimental Parasitology

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Histopathological lesions in encephalon and heart of mice infected with Toxoplasma gondii increase after Lycopodium clavatum 200dH treatment

Pereira

Góis

Lera³

et al. 2017

Pathology - Research and Practice

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Fibrogenesis and collagen resorption in the heart and skeletal muscle of Calomys callosus experimentally infected with Trypanosoma cruzi: immunohistochemical identification of extracellular matrix components

Abstract: Intense inflammatory lesions and early development of interstitial fibrosis of the myocardium and skeletal

Cited by 8 publications

References 18 publications

Regulation and use of the extracellular matrix by Trypanosoma cruzi during early infection

Regulation and use of the extracellular matrix by Trypanosoma cruzi during early infection

Trypanosoma cruzi–cardiomyocyte interaction: role of fibronectin in the recognition process and extracellular matrix expression in vitro and in vivo

Histopathological lesions in encephalon and heart of mice infected with Toxoplasma gondii increase after Lycopodium clavatum 200dH treatment

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