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: 2.86). 06/2011; 13(12-13):1002-5. DOI: 10.1016/j.micinf.2011.06.002
Source: PubMed


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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    • "In the initial steps of infection, T. cruzi enters subcutaneous adipose tissue , a mechanism readily confirmed in infected 3T3-L1 adipocyte culture (Combs et al., 2005; Nagajyothi et al., 2008). Adipose tissue can host T. cruzi for decades, protecting the infected from Chagas disease progression to cardiovascular death (Ferreira et al., 2011; Nagajyothi et al., 2012). Interestingly, Chagas disease increases the incidence of hyperglycemia in human correlation studies and, experimentally , hyperglycemic mice harbor increased parasitic loads and exhibit increased mortality upon T. cruzi infection (Amole et al., 1985; Tanowitz et al., 1988). "
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    ABSTRACT: Adipose tissue is a complex, multicellular organ that profoundly influences the function of nearly all other organ systems through its diverse metabolite and adipokine secretome. Adipocytes are the primary cell type of adipose tissue and play a key role in maintaining energy homeostasis. The efficiency with which adipose tissue responds to whole-body energetic demands reflects the ability of adipocytes to adapt to an altered nutrient environment, and has profound systemic implications. Deciphering adipocyte cell biology is an important component of understanding how the aberrant physiology of expanding adipose tissue contributes to the metabolic dysregulation associated with obesity. © 2015 Rutkowski et al.
    The Journal of Cell Biology 03/2015; 208(5):501-512. DOI:10.1083/jcb.201409063 · 9.83 Impact Factor
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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.
    Mediators of Inflammation 06/2014; 2014(3). DOI:10.1155/2014/912965 · 3.24 Impact Factor
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