High fat diet modulates Trypanosoma cruzi infection associated myocarditis.

Background: Trypanosoma cruzi, the causative agent of Chagas disease, has high affinity for lipoproteins and adipose tissue. Infection results in myocarditis, fat loss and alterations in lipid homeostasis. This study was aimed at analyzing the effect of high fat diet (HFD) on regulating acute T.

Alterations in glucose homeostasis in a murine model of Chagas disease.

Chagas disease, caused by Trypanosoma cruzi, is an important cause of morbidity and mortality primarily resulting from cardiac dysfunction, although T. cruzi infection results in inflammation and cell destruction in many organs. We found that T.

Current understanding of immunity to Trypanosoma cruzi infection and pathogenesis of Chagas disease.

Chagas disease caused by Trypanosoma cruzi remains an important neglected tropical disease and a cause of significant morbidity and mortality. No longer confined to endemic areas of Latin America, it is now found in non-endemic areas due to immigration. The parasite may persist in any tissue, but in recent years, there has been increased recognition of adipose tissue both as an early target of infection and a reservoir of chronic infection.

The vasculature in chagas disease.

The cardiovascular manifestations of Chagas disease are well known. However, the contribution of the vasculature and specifically the microvasculature has received little attention. This chapter reviews the evidence supporting the notion that alterations in the microvasculature especially in the heart contribute to the pathogenesis of chagasic cardiomyopathy.

Aspirin treatment of mice infected with Trypanosoma cruzi and implications for the pathogenesis of Chagas disease.

Chagas disease, caused by infection with Trypanosoma cruzi, is an important cause of cardiovascular disease. It is increasingly clear that parasite-derived prostaglandins potently modulate host response and disease progression. Here, we report that treatment of experimental T.

Crucial role of the central leptin receptor in murine Trypanosoma cruzi (Brazil strain) infection.

Mice carrying a defective leptin receptor gene (db/db mice) are metabolically challenged and upon infection with Trypanosoma cruzi (Brazil strain) suffer high mortality. In genetically modified db/db mice, (NSE-Rb db/db mice), central leptin signaling is reconstituted only in the brain, which is sufficient to correct the metabolic defects. NSE-Rb db/db mice were infected with T.

Lack of association between adiponectin levels and atherosclerosis in mice.

Objective: Adiponectin is an adipocyte-derived, secreted protein that is implicated in protection against a cluster of related metabolic disorders. Mice lacking adiponectin display impaired hepatic insulin sensitivity and respond only partially to peroxisome proliferator-activated receptor gamma agonists. Adiponectin has been associated with antiinflammatory and antiatherogenic properties; however, the direct involvement of adiponectin on the atherogenic process has not been studied.

Perspectives on Trypanosoma cruzi-induced heart disease (Chagas disease).

Chagas disease is caused by the parasite Trypanosoma cruzi. It is a common cause of heart disease in endemic areas of Latin America. The year 2009 marks the 100th anniversary of the discovery of T cruzi infection and Chagas disease by the Brazilian physician Carlos Chagas.

Interferon-alpha treatment of female (NZW x BXSB)F(1) mice mimics some but not all features associated with the Yaa mutation.

Objective: Male (NZW x BXSB)F(1) mice develop antiphospholipid syndrome (APS) and proliferative glomerulonephritis that is markedly accelerated by the Yaa locus encoding an extra copy of Tlr7. Female (NZW x BXSB)F(1) mice with only 1 active copy of Tlr7 develop late-onset glomerulonephritis but not APS. Because a major function of Toll-like receptor 7 is to induce type I interferons (IFNs), our goal was to determine whether IFNalpha can induce or accelerate the manifestations of systemic lupus erythematosus (SLE) in female (NZW x BXSB)F(1) mice.

A magnetic resonance imaging study of intestinal dilation in Trypanosoma cruzi-infected mice deficient in nitric oxide synthase.

Infection with Trypanosoma cruzi causes megasyndromes of the gastrointestinal (GI) tract. We used magnetic resonance imaging (MRI) to monitor alterations in the GI tract of T. cruzi-infected mice, and to assess the role of nitric oxide (NO) in the development of intestinal dilation.

Prevention of murine antiphospholipid syndrome by BAFF blockade.

Objective: This study was undertaken to determine whether BAFF blockade can be used to prevent or treat antiphospholipid syndrome in a mouse model.

Methods: Eight- and 12-week-old (NZW x BXSB)F(1) mice were treated with BAFF-R-Ig or TACI-Ig alone or in addition to a short course of CTLA-4Ig. Mice were monitored for thrombocytopenia and proteinuria.

Amebic colitis in an antigenically and serologically negative patient: usefulness of a small-subunit ribosomal RNA gene-based polymerase chain reaction in diagnosis.

Specific identification of Entamoeba histolytica in clinical specimens is an essential confirmatory diagnostic step in the management of amebiasis. Here, we report an unusual case of amebic colitis in a 20-year-old female immigrant from South China. The patient had experienced diarrhea, crampy abdominal pain, and fever for approximately 3 weeks prior to admission to hospital and had treated herself at home with metronidazole.

Thromboxane A2 is a key regulator of pathogenesis during Trypanosoma cruzi infection.

Chagas' disease is caused by infection with the parasite Trypanosoma cruzi. We report that infected, but not uninfected, human endothelial cells (ECs) released thromboxane A(2) (TXA(2)). Physical chromatography and liquid chromatography-tandem mass spectrometry revealed that TXA(2) is the predominant eicosanoid present in all life stages of T.

Dosage-dependent transcriptional regulation by the calcineurin/NFAT signaling in developing myocardium transition.

Thin spongy myocardium is critical at early embryonic stage [before embryonic day (E) 13.5 in mice] to allow diffusion of oxygen and nutrients to the developing cardiomyocytes. However, establishment of compact myocardium at later stage ( approximately E16.

Limited myocardial muscle necrosis model allowing for evaluation of angiogenic treatment modalities.

The currently accepted model for creating infarcted cardiac tissue in a rat model involves ligation of the left anterior descending artery (LAD), either proximally or at the bifurcation level. This procedure requires significant technical expertise and, even in skilled hands, commonly results in a 30% to 60% animal mortality. The authors propose a new model for creating a limited area of myocardial muscle necrosis that can be effectively studied.

Cell cycle regulatory proteins in the liver in murine Trypanosoma cruzi infection.

The liver is an important target of Trypanosoma cruzi infection. Infection of CD-1 mice with T. cruzi (Brazil strain) resulted in parasitism of the liver, primarily in sinusoidal and Kupffer cells.

Changes in the chemical and dynamic properties of cardiac troponin T cause discrete cardiomyopathies in transgenic mice.

Cardiac troponin T (cTnT) is a central component of the regulatory thin filament. Mutations in cTnT have been linked to severe forms of familial hypertrophic cardiomyopathy. A mutational "hotspot" that leads to distinct clinical phenotypes has been identified at codon 92.

Cyclin and caveolin expression in an acute model of murine Chagasic myocarditis.

Chagas' disease caused by the parasite, Trypanosoma cruzi, is accompanied by an acute myocarditis which can be fatal. Mice (A/J strain) infected with T. cruzi (Tulahuen strain) develop an acute myocarditis associated with high parasitemia and uniform mortality.

The adipocyte as an important target cell for Trypanosoma cruzi infection.

Adipose tissue plays an active role in normal metabolic homeostasis as well as in the development of human disease. Beyond its obvious role as a depot for triglycerides, adipose tissue controls energy expenditure through secretion of several factors. Little attention has been given to the role of adipocytes in the pathogenesis of Chagas disease and the associated metabolic alterations.

Trypanosoma cruzi infection induced changes in the innervation, structure and function of the murine bladder.

Purpose: The involvement of the lower urinary tract in chronic Chagas' disease has received little attention. Therefore, we investigated pathology and functional alterations in the bladder of Trypanosoma cruzi infected mice.

Materials And Methods: CD1 mice were infected with 5 x 10 T.

Role of endothelin 1 in the pathogenesis of chronic chagasic heart disease.

On the basis of previous observations, endothelin 1 (ET-1) has been suggested as contributing to the pathogenesis of Chagasic cardiomyopathy. Therefore, ET-1flox/flox;alpha-MHC-Cre(+) mice in which the ET-1 gene was deleted from cardiac myocytes and ET-1flox/flox;Tie 2 Cre(+) mice in which the ET-1 gene was deleted from endothelial cells were infected with Trypanosoma cruzi. Genetic controls for these cell-specific ET-1 knockout mice were used.

MR imaging of caveolin gene-specific alterations in right ventricular wall thickness.

Caveolin-1 and caveolin-3 are expressed in the mammalian heart. Mice deficient in caveolin 1 or 3 exhibit cardiac abnormalities including left ventricular hypertrophy and reduced fractional shortening. Cardiac imaging technologies such as transthoracic echocardiography and cardiac-gated magnetic resonance imaging (MRI) are effective tools for the study of left ventricular morphology and function in mice; however, there has not been widespread use of these technologies in studies of right ventricular morphology.

CTLA4Ig prevents initiation but not evolution of anti-phospholipid syndrome in NZW/BXSB mice.

NZW "x" BXSB F1 mice develop SLE that is associated with an anti-phospholipid syndrome characterized by anti-cardiolipin antibodies, thrombocytopenia and small coronary artery thrombosis. This syndrome is immune mediated and, dependent, on CD4+T cells. To determine whether disease in these mice can be treated with blockade of T cell costimulation we treated them with the CD28 antagonist CTLA4Ig at 9 or 12 weeks of age.

Effects of early and late verapamil administration on the development of cardiomyopathy in experimental chronic Trypanosoma cruzi (Brazil strain) infection.

Chagas' disease, caused by Trypanosoma cruzi, leads to acute myocarditis and chronic cardiomyopathy. Myocardial structure and function were evaluated in T. cruzi (Brazil strain)-infected CD1 mice by histopathology, cardiac gated magnetic resonance imaging (MRI) and transthoracic echocardiography.

Urogenital alterations in aged male caveolin-1 knockout mice.

Purpose: Caveolae are flask-shaped invaginations of the plasma membrane formed by the oligomerization of caveolins. Because only smooth muscle contains all caveolin (Cav) family members (Cav-1, 2 and 3), we examined the contribution of each caveolin to urogenital smooth muscle structure/function.

Materials And Methods: WT, Cav-1, 2, 3 and -1/3 knockout (KO) mouse bladders were characterized by Western blot, co-immunoprecipitation, immunofluorescence microscopy, electron microscopy, histochemistry and pharmacological techniques.