Comparative pathogenicity in Swiss mice of Trypanosoma cruzi IV from northern Brazil and Trypanosoma cruzi II from southern Brazil

Meza, Sheila Karina Lüders; Kaneshima, Edílson Nobuyoshi; Silva, Sueli de Oliveira; Gabriel, Maristela; Araújo, Silvana Márques de; Gomes, Mônica Lúcia; Monteiro, Wuelton Marcelo; Barbosa, Maria das Graças Vale; Toledo, Max Jean de Ornelas

doi:10.1016/j.exppara.2014.08.014

Cited by 26 publications

(19 citation statements)

References 31 publications

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“…More recently, our group experimentally demonstrated that cardiac an renal manifestations of CD were associated with the parasite burden and the inflammation resulting from infection [ 15 , 16 ], and these findings suggest that changes in other organs such as the intestine might be also affected by the same parameters. Lately it has been rated the strains of T. cruzi according to their genetic characteristics, and our work reinforces that besides the pathogenic characteristics attributed to each Discrete Typing Unit (DTU) of T. cruzi [ 17 - 19 ], it is also important to consider the concentration of the inoculum in the induction of these intestinal disease processes.…”

Section: Introductionsupporting

confidence: 67%

Inflammatory responses and intestinal injury development during acute Trypanosoma cruzi infection are associated with the parasite load

Vazquez

Miguel

et al. 2015

Parasites Vectors

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BackgroundChagas disease is caused by the protozoan Trypanosoma cruzi and is characterized by cardiac, gastrointestinal, and nervous system disorders. Although much about the pathophysiological process of Chagas disease is already known, the influence of the parasite burden on the inflammatory process and disease progression remains uncertain.MethodsWe used an acute experimental disease model to evaluate the effect of T. cruzi on intestinal lesions and assessed correlations between parasite load and inflammation and intestinal injury at 7 and 14 days post-infection. Low (3 × 102), medium (3 × 103), and high (3 × 104) parasite loads were generated by infecting C57BL/6 mice with “Y”-strain trypomastigotes. Statistical analysis was performed using analysis of variance with Tukey’s multiple comparison post-test, Kruskal–Wallis test with Dunn’s multiple comparison, χ2 test and Spearman correlation.ResultsHigh parasite load-bearing mice more rapidly and strongly developed parasitemia. Increased colon width, inflammatory infiltration, myositis, periganglionitis, ganglionitis, pro-inflammatory cytokines (e.g., TNF-α, INF-γ, IL-2, IL-17, IL-6), and intestinal amastigote nests were more pronounced in high parasite load-bearing animals. These results were remarkable because a positive correlation was observed between parasite load, inflammatory infiltrate, amastigote nests, and investigated cytokines.ConclusionsThese experimental data support the idea that the parasite load considerably influences the T. cruzi-induced intestinal inflammatory response and contributes to the development of the digestive form of the disease.

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Section: Introductionsupporting

confidence: 67%

Inflammatory responses and intestinal injury development during acute Trypanosoma cruzi infection are associated with the parasite load

Vazquez

Miguel

et al. 2015

Parasites Vectors

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“…Since the first description of American trypanosomiasis by Dr. Carlos Chagas, increasing evidence indicate the complexity of this human disease, although the reasons for this are not entirely clear yet 1 , 2 . Moreover, few studies in animal models have scarcely addressed this heterogeneity and few studies have been performed with more than 2 different strains 6 , 12 , 14 , 18 , 26 , 27 . To address the heterogeneity of CD, we infected animals with 6 T. cruzi strains – one from each DTU of the species – and analyzed 66 markers related to the pathophysiogenesis, thus covering a wide range of host responses in a multi-parametric approach.…”

Section: Discussionmentioning

confidence: 99%

“…Trees do not allow seeing the wood: heterogeneity of responses to T. cruzi at immunological and pathophysiological levels was described both in murine models 16 , 26 , 27 , 34 and patients 23 but not clearly integrated into a model compliant with clinical situations. For instance, the same treatment is applied to all infected humans regardless of the clinical manifestations or the infecting strains, despite knowing that all strains may not be equally susceptible to drugs 35 , 36 .…”

Section: Discussionmentioning

confidence: 99%

A multi-parametric analysis of Trypanosoma cruzi infection: common pathophysiologic patterns beyond extreme heterogeneity of host responses

Santi-Rocca

Fernández-Cortés

Chillón-Marinas

et al. 2017

Sci Rep

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The extreme genetic diversity of the protozoan Trypanosoma cruzi has been proposed to be associated with the clinical outcomes of the disease it provokes: Chagas disease (CD). To address this question, we analysed the similarities and differences in the CD pathophysiogenesis caused by different parasite strains. Using syngeneic mice infected acutely or chronically with 6 distant parasite strains, we integrated simultaneously 66 parameters: parasite tropism (7 parameters), organ and immune responses (local and systemic; 57 parameters), and clinical presentations of CD (2 parameters). While the parasite genetic background consistently impacts most of these parameters, they remain highly variable, as observed in patients, impeding reliable one-dimensional association with phases, strains, and damage. However, multi-dimensional statistics overcame this extreme intra-group variability for each individual parameter and revealed some pathophysiological patterns that accurately allow defining (i) the infection phase, (ii) the infecting parasite strains, and (iii) organ damage type and intensity. Our results demonstrated a greater variability of clinical outcomes and host responses to T. cruzi infection than previously thought, while our multi-parametric analysis defined common pathophysiological patterns linked to clinical outcome of CD, conserved among the genetically diverse infecting strains.

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“…24,25 The genetic characteristics of the parasites or hosts are pivotal aspects for the establishment of a diffuse cellular infiltration composed mainly of mononuclear cells and lymphocytes. 5,[26][27][28] This pattern will contribute to the pathogenesis of cardiac lesions because of 1) the disruption and displacement of local vascular beads and the cardiac myofibrils, 2) the collagen deposition in the heart followed by fibrosis, and 3) the remodeling and loss of functionality of the heart in human and in experimental models. Therefore, the elimination of the parasites is an obvious interest of chemical therapy because of the persistent antigenic stimulation caused to the mammalian host.…”

Section: Discussionmentioning

confidence: 99%

Enalapril in Combination with Benznidazole Reduces Cardiac Inflammation and Creatine Kinases in Mice Chronically Infected with Trypanosoma cruzi

Penitente¹,

Leite²,

Costa³

et al. 2015

The American Society of Tropical Medicine and Hygiene

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Comparative pathogenicity in Swiss mice of Trypanosoma cruzi IV from northern Brazil and Trypanosoma cruzi II from southern Brazil

Cited by 26 publications

References 31 publications

Inflammatory responses and intestinal injury development during acute Trypanosoma cruzi infection are associated with the parasite load

Inflammatory responses and intestinal injury development during acute Trypanosoma cruzi infection are associated with the parasite load

A multi-parametric analysis of Trypanosoma cruzi infection: common pathophysiologic patterns beyond extreme heterogeneity of host responses

Enalapril in Combination with Benznidazole Reduces Cardiac Inflammation and Creatine Kinases in Mice Chronically Infected with Trypanosoma cruzi

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