Trypanosoma cruzi strains in the Calomys callosus: parasitemia and reaction of intracellular forms with stage-specific antibodies in the acute and chronic phase of infection and after immunosuppression

2011 ◽  
Vol 109 (2) ◽  
pp. 431-440 ◽  
Author(s):  
Noemi Nosomi Taniwaki ◽  
Viviane Martinelli Gonçalves ◽  
Julianna Kesselring Romero ◽  
Claudio Vieira da Silva ◽  
Solange da Silva ◽  
...  
Keyword(s):  
Trypanosoma Cruzi ◽  
Chronic Phase ◽  
Specific Antibodies ◽  
Calomys Callosus

Combined treatment with benznidazole and allopurinol in mice infected with a virulentTrypanosoma cruziisolate from Nicaragua

Parasitology ◽  
2013 ◽  
Vol 140 (10) ◽  
pp. 1225-1233 ◽  
Author(s):  
NOELIA L. GROSSO ◽  
MICAELA LOPEZ ALARCON ◽  
JAQUELINE BUA ◽  
SUSANA A. LAUCELLA ◽  
ADELINA RIARTE ◽  
...  
Keyword(s):  
Survival Rate ◽  
Trypanosoma Cruzi ◽  
Endemic Area ◽  
Low Dose ◽  
Combined Treatment ◽  
Chronic Phase ◽  
Experimental Models ◽  
Specific Antibodies ◽  
Histopathological Studies ◽  
Virulent Parasite

SUMMARYWe evaluated the effect of chemotherapy with a sequential combined treatment of a low dose of benznidazole and allopurinol, in different schedules of administration, in experimental models of acute and chronicTrypanosoma cruziinfection. Mice were infected with NicaraguaT. cruziisolate, a virulent parasite from an endemic area of Nicaragua, genotyped asTcI (Grossoet al. 2010). We assessed survival rate, IgG levels, histopathological studies and quantified parasitaemia. A 15% survival rate was recorded in untreated mice during the acute phase ofT. cruziinfection. Allopurinol administered immediately after benznidazole treatment was able to reduce parasitaemia and attenuate tissue damage by reducing inflammation.Trypanosoma cruzi-specific antibodies also decreased in 40–50% of the treated mice. The addition of allopurinol during the chronic phase showed the highest beneficial effect, not only by reducing parasitaemia but also by lowering the degree of inflammation and fibrosis.

Dynamics of T Cells Repertoire During Trypanosoma cruzi Infection and its Post-Treatment Modulation

2019 ◽  
Vol 26 (36) ◽  
pp. 6519-6543 ◽  
Author(s):  
Adriana Egui ◽  
Paola Lasso ◽  
Elena Pérez-Antón ◽  
M. Carmen Thomas ◽  
Manuel Carlos López
Keyword(s):  
Immune Response ◽  
Trypanosoma Cruzi ◽  
Chagas Disease ◽  
Cardiac Tissue ◽  
Acute Infection ◽  
Clinical Status ◽  
Chronic Phase ◽  
Parasite Load ◽  
Chronic Patients ◽  
Cruzi Infection

Chagas disease courses with different clinical phases and has a variable clinical presentation and progression. The acute infection phase mostly exhibits a non-specific symptomatology. In the absence of treatment, the acute phase is followed by a chronic phase, which is initially asymptomatic. This chronic asymptomatic phase of the disease is characterized by a fragile balance between the host’s immune response and the parasite replication. The loss of this balance is crucial for the progression of the sickness. The virulence and tropism of the T. cruzi infecting strain together to the inflammation processes in the cardiac tissue are the main factors for the establishment and severity of the cardiomyopathy. The efficacy of treatment in chronic Chagas disease patients is controversial. However, several studies carried out in chronic patients demonstrated that antiparasitic treatment reduces parasite load in the bloodstream and leads to an improvement in the immune response against the Trypanosoma cruzi parasite. The present review is mainly focused on the cellular patterns associated to the clinical status and the evolution of the disease in chronic patients, as well as the effectiveness of the treatment related to T. cruzi infection control. Therefore, an emphasis is placed on the dynamics of specific-antigens T cell subpopulations, their memory and activation phenotypes, their functionality and their contribution to pathogenesis or disease control, as well as their association with risk of congenital transmission of the parasite.

Parasite Specific Antibodies in Three Strains of Mice after Infection with Trypanosoma cruzi

1985 ◽  
Vol 71 (1) ◽  
pp. 43 ◽  
Author(s):  
Hans J. Zweerink ◽  
O. Fred Anderson ◽  
Hellen C. Greenblatt ◽  
P. Keith Murray
Keyword(s):  
Trypanosoma Cruzi ◽  
Specific Antibodies

Is nitric oxide involved in the tolerance of Calomys callosus as a reservoir host towards Trypanosoma cruzi infection?

2006 ◽  
Vol 52 (1) ◽  
pp. 49-55 ◽  
Author(s):  
C DOST ◽  
J SARAIVA ◽  
U ZENTGRAF ◽  
N MONESI ◽  
W ENGELS ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Trypanosoma Cruzi ◽  
Reservoir Host ◽  
Calomys Callosus ◽  
Cruzi Infection

Abstract 83: Modulation of Macrophage Function via Metabolism by Trypanosoma cruzi

2015 ◽  
Vol 117 (suppl_1) ◽  
Author(s):  
Sue-Jie Koo ◽  
Nisha J Garg
Keyword(s):  
Trypanosoma Cruzi ◽  
Chronic Phase ◽  
Etiologic Agent ◽  
Acid Oxidation ◽  
Peroxisome Proliferator ◽  
Transcription Control ◽  
Metabolic Gene Expression ◽  
Anti Inflammatory ◽  
Peroxisome Proliferator Activated Receptors ◽  
The Impact

Chagas heart disease is an inflammatory cardiomyopathy which presents with mononuclear infiltrates in the interstitium and myocardial fibrosis in the chronic phase. Incomplete clearance by macrophages of the etiologic agent, Trypanosoma cruzi , is a significant cause of chronic disease development in approximately 30% of those serologically positive for the blood-borne parasite. The differential metabolic status, anaerobic glycolysis and mitochondria-dependent oxidative phosphorylation, are respectively associated with pro-inflammatory (M1) and anti-inflammatory (M2) functional activation of macrophages. Reactive oxygen species (ROS) have been shown to be an intracellular signal for glycolysis while peroxisome proliferator-activated receptors (PPARs) that enhance fatty acid oxidation provide transcription control of macrophage functional state. In our studies using diverse T. cruzi isolates, we showed that SylvioX10 (virulent), but not TCC (non-virulent), isolates are able to differentially control extracellular and intracellular ROS levels in macrophages. We found in macrophages infected with SylvioX10, the nuclear expression of PPAR-α was increased by 18 hours post-infection, and mitochondrial metabolic activity was similar to that of not-infected and M2 controls; which indicates anti-inflammatory function of macrophages, and therefore prohibiting T. cruzi clearance. In our ongoing studies, we are examining the impact of PPAR-α inhibitors in modulating the metabolic gene expression profile, functional phenotype and parasite survival in macrophages. Our data will provide the first indication that host macrophages have deficient pro-inflammatory capacity due to sub-optimal glucose oxidation, and enhancing the metabolism that supports T. cruzi clearance will provide a valuable basis for a strategy to arrest Chagas disease progression.

scholarly journals Immunoblotting analyses using two-dimensional gel electrophoresis of Trypanosoma cruzi excreted-secreted antigens

2004 ◽  
Vol 37 (6) ◽  
pp. 454-459
Author(s):  
Adriano Gomes Silva ◽  
Elisangela Paula Silveira-Lacerda ◽  
Jair Pereira Cunha-Júnior ◽  
Maria Aparecida de Souza ◽  
Silvio Favoreto Junior
Keyword(s):  
Trypanosoma Cruzi ◽  
Chagas Disease ◽  
Gel Electrophoresis ◽  
Complex Mixture ◽  
Chronic Phase ◽  
Disease Diagnosis ◽  
Basic Knowledge ◽  
Two Dimensional ◽  
Two Dimensional Gel Electrophoresis ◽  
Secreted Antigens

Trypanosoma cruzi trypomastigotes excrete-secrete a complex mixture of antigenic molecules. This antigenic mixture denominated trypomastigote excreted-secreted antigens contains a 150-160 kDa band that shows excellent performance in Chagas' disease diagnosis by immunoblotting. The present study partially characterized by two-dimensional gel electrophoresis the immunoreactivity against the 150-160kDa protein using sera samples from chagasic patients in different phases of the disease. Trypomastigote excreted-secreted antigen preparations were subjected to high-resolution two-dimensional (2D) gel electrophoresis followed by immunoblotting with sera from chagasic and non-chagasic patients. The 150-160kDa protein presented four isoforms with isoelectric focusing ranging from 6.2 to 6.7. The four isoforms were recognized by IgM from acute phase and IgG from chronic phase sera of chagasic patients. The 150-160kDa isoform with IF of approximately 6.4 became the immunodominant spot with the progression of the disease. No cross-reactivity was observed with non-chagasic or patients infected with Leishmania sp. In this study we provide basic knowledge that supports the validation of trypomastigote excreted-secreted antigens for serological diagnosis of Chagas' disease.

scholarly journals Infection of Calomys callosus (Rodentia Cricetidae) with strains of different Trypanosoma cruzi biodemes: pathogenicity, histotropism, and fibrosis induction

2004 ◽  
Vol 99 (4) ◽  
pp. 407-413 ◽  
Author(s):  
Isis Fernandes Magalhães-Santos ◽  
Márcia Maria Souza ◽  
Carolina Silva Costa Lima ◽  
Sonia G Andrade
Keyword(s):  
Trypanosoma Cruzi ◽  
Calomys Callosus

scholarly journals Neuronal changes caused by Trypanosoma cruzi: an experimental model

2011 ◽  
Vol 83 (2) ◽  
pp. 545-555 ◽  
Author(s):  
Neide M Moreira ◽  
Débora M. G Sant'ana ◽  
Eduardo J. A Araújo ◽  
Max J. O Toledo ◽  
Mônica L Gomes ◽  
...  
Keyword(s):  
Trypanosoma Cruzi ◽  
Experimental Model ◽  
Morphometric Analysis ◽  
Chronic Phase ◽  
Post Inoculation ◽  
Male Mice ◽  
Neuronal Density ◽  
Myenteric Neurons ◽  
Time Of Infection ◽  
Neuronal Hypertrophy

Define an experimental model by evaluating quantitative and morphometric changes in myenteric neurons of the colon of mice infected with Trypanosoma cruzi. Twenty-eight Swiss male mice were distributed into groups: control (CG, n=9) and inoculated with 100 (IG100, n=9) and 1000 (IG1000, n=10) blood trypomastigotes, Y strain-T. cruzi II. Parasitemia was evaluated from 3-25 days post inoculation (dpi) with parasites peak of 7.7 × 10(6) and 8.4 × 10(6) trypomastigotes/mL at 8th dpi (p>0.05) in IG100 and IG1000, respectively. Chronic phase of the infection was obtained with two doses of 100mg/Kg/weight and one dose of 250mg/Kg/weight of Benznidazole on 11, 16 and 18 dpi. Three animals from each group were euthanized at 18, 30 and 75 dpi. The colon was stained with Giemsa. The quantitative and morphometric analysis of neurons revealed that the infection caused a decrease of neuronal density on 30th dpi (p<0.05) and 75 dpi (p<0.05) in IG100 and IG1000. Infection caused death and neuronal hypertrophy in the 75th dpi in IG100 and IG1000 (p<0.05, p<0.01). The changes observed in myenteric neurons were directly related to the inoculate and the time of infection

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