Article

Evidence for Trypanosoma cruzi in adipose tissue in human chronic Chagas disease

Department of Basic Nursing, Nursing School, Universidade Federal de Minas Gerais, Belo Horizonte 31270-901, Brazil.
Microbes and Infection (Impact Factor: 2.73). 06/2011; 13(12-13):1002-5. DOI: 10.1016/j.micinf.2011.06.002
Source: PubMed

ABSTRACT Trypanosoma cruzi the cause of Chagas disease persists in tissues of infected experimental animals and humans. Here we demonstrate the persistence of the parasite in adipose tissue from of three of 10 elderly seropositive patients with chronic chagasic heart disease. Nine control patients had no parasites in the fat. We also demonstrate that T. cruzi parasitizes primary adipocytes in vitro. Thus, in humans as in mice the parasite may persist in adipose tissue for decades and become a reservoir of infection.

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Available from: Marcela Segatto, Aug 29, 2015
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    • "These findings suggest that adipose tissues may serve as the parasitic reservoir during chronic infection and adipokine synthesis was disrupted possibly due to the infection [54]. Observations that T. cruzi parasite is present in the adipose tissue biopsy of chronically infected human patients have further confirmed the finding that adipose tissue is the reservoir of chronic T. cruzi infection [55]. Several follow-up studies have also shown the susceptible nature of adipocytes to T. cruzi infection [8, 56]. "
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    ABSTRACT: Trypanosoma cruzi is the causative agent of Chagas disease. Approximately 8 million people are thought to be affected worldwide. Several players in host lipid metabolism have been implicated in T. cruzi-host interactions in recent research, including macrophages, adipocytes, low density lipoprotein (LDL), low density lipoprotein receptor (LDLR), and high density lipoprotein (HDL). All of these factors are required to maintain host lipid homeostasis and are intricately connected via several metabolic pathways. We reviewed the interaction of T. cruzi with each of the relevant host components, in order to further understand the roles of host lipid metabolism in T. cruzi infection. This review sheds light on the potential impact of T. cruzi infection on the status of host lipid homeostasis.
    Mediators of Inflammation 09/2014; 2014:902038. DOI:10.1155/2014/902038 · 3.24 Impact Factor
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    • "One of these parasite niches could be the central adrenal vein, which, in autopsy studies of patients with chronic Chagas disease, has been found to frequently harbor amastigote nests; further, the presence of these nests shows a close correlation with heart pathology parameters such as the intensity of leukocyte infiltration and myocardial fibrosis [50]. Additionally, both brown and white adipose tissues, as well as the colon and stomach, have been described as locations where T. cruzi parasites chronically persist [49, 51, 52]. Moreover, because of parasite persistence in the cardiac tissue of CCC patients, the heart could be one of these niches for a fraction of the infected population. "
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    ABSTRACT: Over the past 20 years, the immune effector mechanisms involved in the control of Trypanosoma cruzi , as well as the receptors participating in parasite recognition by cells of the innate immune system, have been largely described. However, the main questions on the physiopathology of Chagas disease remain unanswered: “Why does the host immune system fail to provide sterile immunity?” and “Why do only a proportion of infected individuals develop chronic pathology?” In this review, we describe the mechanisms proposed to explain the inability of the immune system to eradicate the parasite and the elements that allow the development of chronic heart disease. Moreover, we discuss the possibility that the inability of infected cardiomyocytes to sense intracellular T. cruzi contributes to parasite persistence in the heart and the development of chronic pathology.
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    • "In these long-term infections, most parasites are intracellular replicative amastigotes, and existing evidence indicates that they reside predominantly in muscle tissues (Zhang and Tarleton, 1999). Adipocytes have been suggested as a possible secondary reservoir site (Matos Ferreira et al., 2011; Nagajyothi et al., 2012). End-point assays such as histology, PCR and serology require large animal cohorts and the utility of such data is typically limited by tissue sampling biases and the focal nature of tissue infections. "
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    ABSTRACT: Chronic Trypanosoma cruzi infections lead to cardiomyopathy in 20-30% of cases. A causal link between cardiac infection and pathology has been difficult to establish because of a lack of robust methods to detect scarce, focally distributed parasites within tissues. We developed a highly sensitive bioluminescence imaging system based on T. cruzi expressing a novel luciferase that emits tissue-penetrating orange-red light. This enabled long-term serial evaluation of parasite burdens in individual mice with an in vivo limit of detection of significantly less than 1000 parasites. Parasite distributions during chronic infections were highly focal and spatiotemporally dynamic, but did not localize to the heart. End-point ex vivo bioluminescence imaging allowed tissue-specific quantification of parasite loads with minimal sampling bias. During chronic infections, the gastro-intestinal tract, specifically the colon and stomach, was the only site where T. cruzi infection was consistently observed. Quantitative PCR-inferred parasite loads correlated with ex vivo bioluminescence and confirmed the gut as the parasite reservoir. Chronically infected mice developed myocarditis and cardiac fibrosis, despite the absence of locally-persistent parasites. These data identify the gut as a permissive niche for long-term T. cruzi infection and show that canonical features of Chagas disease can occur without continual myocardium-specific infection.
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