A role for extracellular amastigotes in the immunopathology of Chagas disease

Scharfstein, Júlio; Morrot, Alexandre

doi:10.1590/s0074-02761999000700005

Cited by 31 publications

(27 citation statements)

References 86 publications

(60 reference statements)

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“…Also, a new class of T. cruzi molecules has been reported to play a crucial role facilitating parasite mobilization through the ECM. These T. cruzi ECM-binding proteins, including the 51 kDa cysteine proteinase cruzipain, present enzymatic activity and mediate type I collagen and FN degradation (8,9). In vivo, cruzipain also binds to the FN network present in the heart tissue of T. cruzi-infected mice (Figure 1), as previously demonstrated among the T. cruzi antigens released into the cardiac interstitial spaces of chagasic patients (10).…”

Section: Trypanosoma Cruzi-host Cell Interactionmentioning

confidence: 62%

Trypanosoma cruzi infection: a continuous invader-host cell cross talk with participation of extracellular matrix and adhesion and chemoattractant molecules

Marino¹,

Silva²,

Pinho

et al. 2003

Braz J Med Biol Res

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Several lines of evidence have shown that Trypanosoma cruzi interacts with host extracellular matrix (ECM) components producing breakdown products that play an important role in parasite mobilization and infectivity. Parasite-released antigens also modulate ECM expression that could participate in cell-cell and/or cell-parasite interactions. Increased expression of ECM components has been described in the cardiac tissue of chronic chagasic patients and diverse target tissues including heart, thymus, central nervous system and skeletal muscle of experimentally T. cruzi-infected mice. ECM components may adsorb parasite antigens and cytokines that could contribute to the establishment and perpetuation of inflammation. Furthermore, T. cruzi-infected mammalian cells produce cytokines and chemokines that not only participate in the control of parasitism but also contribute to the establishment of chronic inflammatory lesions in several target tissues and most frequently lead to severe myocarditis. T. cruzi-driven cytokines and chemokines may also modulate VCAM-1 and ICAM-1 adhesion molecules on endothelial cells of target tissues and play a key role in cell recruitment, especially of activated VLA-4 + LFA-1 + CD8 + T lymphocytes, resulting in a predominance of this cell population in the inflamed heart, central nervous system and skeletal muscle. The VLA-4 + -invading cells are surrounded by a fine network of fibronectin that could contribute to cell anchorage, activation and effector functions. Since persistent "danger signals" triggered by the parasite and its antigens are required for the establishment of inflammation and ECM alterations, therapeutic interventions that control parasitism and selectively modulate cell migration improve ECM abnormalities, paving the way for the development of new therapeutic strategies improving the prognosis of T. cruzi-infected individuals.

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Section: Trypanosoma Cruzi-host Cell Interactionmentioning

confidence: 62%

Trypanosoma cruzi infection: a continuous invader-host cell cross talk with participation of extracellular matrix and adhesion and chemoattractant molecules

Marino¹,

Silva²,

Pinho

et al. 2003

Braz J Med Biol Res

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“…Possibly, the destruction of collagen IV around fetal endothelium is not necessary for the parasite invasion of fetal capillaries or occurs at a later time (Duaso et al, 2010). In other studies, an increase of laminin expression in cardiac tissue has been reported (Scharfstein and Morrot, 1999;Marino et al, 2003). The increase of laminin expression could be induced by the parasite, which needs to attach to ECM molecules for cellular invasion (Marino et al, 2003).…”

Section: Trypanosoma Cruzi Interaction With the Villous Stromamentioning

confidence: 96%

“…The silencing of the laminin gene inhibits cell invasion of the T. cruzi (Nde et al, 2006). The parasitic protease cruzipain degrades collagen IV and fibronectin, exposing epitopes to which T. cruzi binds (Scharfstein and Morrot, 1999), facilitating also the binding to laminin and consequently the cell invasion. On the other hand, the breakdown of the ECM facilitates the penetration of the parasite through basal lamina and connective tissue of villous stroma.…”

Section: Trypanosoma Cruzi Interaction With the Villous Stromamentioning

confidence: 99%

Mechanism of Congenital Chagas Disease: Effective Infection Depends on the Interplay Between Trypanosoma cruzi and the Different Tissue Compartments in the Chorionic Villi of the Human Placenta

Duaso¹,

Castillo²,

Kemmerling³

2012

Recent Advances in Research on the Human Placenta

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“…The parasite secretes proteases (cruzipains) capable of degrading ECM components such as collagen type I, IV and fibronectin, exposing hidden epitopes (Santana, et al 1997;Scharfstein and Morrot 1999). Plasma fibronectin fragments have a growth factor type activity that induces differentiation of trypomastigotes into their intracellular replicative form, amastigotes (Ouaissi, et al 1992).…”

Section: T Cruzi Interaction With the Host Ecmmentioning

confidence: 99%

Infection and invasion mechanisms of Trypanosoma cruzi in the congenital transmission of Chagas' disease: A proposal

2010

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Chagas' disease is produced by the haemophlagelated protozoan Trypanosoma cruzi and transmitted by haematophages insects such as Triatoma infestans (vinchuca). Due to vector control, congenital transmission gains importance and is responsible for the presence and expansion of this disease in non-endemic areas. The mechanisms of congenital infection are uncertain. It has been suggested that the parasite reaches the fetus through the bloodstream by crossing the placental barrier, and that congenital Chagas' disease is the result of complex interactions between the immune response, placental factors, and the parasite's characteristics. We review the cellular and molecular mechanisms of infection and invasion of the parasite and how immune and placental factors may modulate this process. Finally, we propose a possible model for the vertical transmission of Chagas´ disease.

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A role for extracellular amastigotes in the immunopathology of Chagas disease

Cited by 31 publications

References 86 publications

Trypanosoma cruzi infection: a continuous invader-host cell cross talk with participation of extracellular matrix and adhesion and chemoattractant molecules

Trypanosoma cruzi infection: a continuous invader-host cell cross talk with participation of extracellular matrix and adhesion and chemoattractant molecules

Mechanism of Congenital Chagas Disease: Effective Infection Depends on the Interplay Between Trypanosoma cruzi and the Different Tissue Compartments in the Chorionic Villi of the Human Placenta

Infection and invasion mechanisms of Trypanosoma cruzi in the congenital transmission of Chagas' disease: A proposal

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