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

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.

Human cytomegalovirus infection of human adipose-derived stromal/stem cells restricts differentiation along the adipogenic lineage

“…Consequently, adipose tissue has been suggested to be a reservoir for specific infectious agents. [12][13][14][15] Human cytomegalovirus (HCMV), a member of the b-herpesvirus family, is one of the most common viruses infecting adults, with the seropositive rate ranging from 60-99% globally. 16 It typically presents as an asymptomatic infection in healthy individuals but can be life-threatening in immunocompromised individuals such as organ and bone marrow transplant patients or individuals positive for HIV/ AIDS.…”

Impact of Chagas Disease on Human Evolution: The Challenges Continue

“…Some authors also report that it's an imbalance in the process of regulation between the pro and anti-inflammatory cytokines, increasing the chances of tissue damage for the person (Combs et al, 2005;Nagajyothi et al, 2009;Ferreira et al, 2011;Tanowitz et al, 2011;Nagajyothi et al, 2012).…”

Dysregulated Network of Immune, Endocrine and Metabolic Markers is Associated to More Severe Human Chronic Chagas Cardiomyopathy

“…There is evidence on the possible contribution of adipose tissue to T. cruzi-induced pathology in mice, but many of them are focused in the acute phase of infection [15][16][17][18][19]. Nevertheless, when considering that the adipose tissue seems to be one of the main reservoirs of T. cruzi during the chronic phase of disease [20], the possibility that a disbalance between certain fat inflamed-derived metabolic factors (like TNF-α, IL-6, leptin and adiponectin) as contributing to cardiomyopathy progression and severity, sounds likely. For instance, unbalanced adipocytokines were associated with the presence of sympathetic dysfunctions in patients with CCC [21].…”