Maria Angélica de Faria Domingues de Lima

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We found that Trypanosoma cruzi trypomastigote cloned surface ligand (gp83 trans-sialidase) signals human macrophages to up-regulate parasite entry by inducing tyrosine phosphorylation of MAP kinase. Preincubation of human macrophages with r-gp83 transsialidase significantly enhanced both the percentage of phagocytosed trypanosomes and the number of(More)
We found that Trypanosoma cruzi trypomastigote cloned surface ligand (gp83 trans-sialidase) signals macrophages to up-regulate parasite entry by activating protein kinase C (PKC). Incubation of r-gp83 ligand with macrophages activates PKC and this activation is abolished when r-gp83 is depleted by immunoprecipitation with anti-r-gp83 antibodies, which(More)
Human defensins play a fundamental role in the initiation of innate immune responses to some microbial pathogens. Here we show that human defensin alpha-1 displays a trypanocidal role against Trypanosoma cruzi, the causative agent of Chagas' disease. The toxicity of human defensin alpha-1 against T. cruzi is mediated by membrane pore formation and the(More)
We have cloned blood trypomastigotes from infected mice and found that Trypanosoma cruzi strains are composed of heterogeneous populations that dramatically vary (more than 100 fold) in their abilities to attach to and enter rat heart myoblasts. Trypomastigote clones were distinctively separated into highly and weakly infective groups presenting higher and(More)
A set of monoclonal antibodies that recognizes a Trypanosoma cruzi 45-kDa protein was produced and used to characterize this molecule and study its role in trypanosome adhesion to heart myoblasts. We found that the 45-kDa protein is a surface mucin, is expressed only in invasive trypomastigotes, but not in noninvasive epimastigotes or amastigotes, and is(More)
This paper describes a new role for the cysteine-cysteine (CC) chemokines RANTES, MIP-1alpha, and MIP-1beta on human macrophage function, which is the induction of nitric oxide (NO)-mediated trypanocidal activity. In a previous report, we showed that RANTES, MIP-1alpha and MIP-1beta enhance Trypanosoma cruzi uptake and promote parasite killing by human(More)
Chagas disease is caused by the parasite Trypanosoma cruzi. The critical initial event is the interaction of the trypomastigote form of the parasite with host receptors. This review highlights recent observations concerning these interactions. Some of the key receptors considered are those for thromboxane, bradykinin, and for the nerve growth factor TrKA.(More)
Trypanosoma cruzi, the causative agent of Chagas heart disease, infects heart and other cells leading to cardiac arrest frequently followed by death. The disease affects millions of individuals in the Americas and is posing health problems because of blood transmission in the US due to large Latin American immigration. Since the current drugs present(More)
We purified a soluble gp83 trans-sialidase (gp83-TSA), from phospholipase C-treated Trypanosoma cruzi trypomastigote membranes, which binds to myoblasts, fibroblasts and macrophages to mediate trypanosome entry. Myoblasts display a single class of receptors for the gp83-TSA present at 4x10(4) per myoblast with a K(d) of 8 nM. Monovalent Fab fragments of the(More)
It is thought that Trypanosoma cruzi, the protozoan that causes Chagas' disease, modulates the extracellular matrix network to facilitate infection of human cells. However, direct evidence to document this phenomenon is lacking. Here we show that the T. cruzi gp83 ligand, a cell surface trans-sialidase-like molecule that the parasite uses to attach to host(More)