Chagas disease, adipose tissue and the metabolic syndrome

Nagajyothi, Fnu; Desruisseaux, Mahalia S.; Weiss, Louis M.; Chua, Streamson C.; Albanese, Chris; Machado, Fabiana S.; Esper, Lísia; Lisanti, Michael P.; Teixeira, Mauro Martins; Scherer, Philipp E.; Tanowitz, Herbert B.

doi:10.1590/s0074-02762009000900028

Cited by 35 publications

(23 citation statements)

References 49 publications

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“…In the present paper, we demonstrate that treatment with 15d-PGJ 2 reduces inflammatory infiltration and decreases the size of amastigote nests in the cardiac tissue of T. cruzi-infected animals. A previous study has demonstrated that T. cruzi infection leads to a reduced expression of adiponectin and PPAR-γ and that this reduction perpetuates the inflammatory phenotype found in CD (Nagajyothi et al 2009). Thus, the use of 15d-PGJ 2 to control the inflammatory response associated with CD may be useful.…”

Section: Discussionmentioning

confidence: 94%

15d-PGJ2 modulates acute immune responses to Trypanosoma cruzi infection

Rodrigues

Miguel

Chica

et al. 2010

Mem. Inst. Oswaldo Cruz

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The acute phase of Trypanosoma cruzi infection is associated with a strong inflammatory reaction in the heart characterised by a massive infiltration of immune cells that is dependent on the T. cruzi strain and the host response. 15d-PGJ2 belongs to a new class of anti-inflammatory compounds with possible clinical applications. We evaluated the effects of 15d-PGJ2 administered during the acute phase of T. cruzi infection in mice. Mice were infected with the Colombian strain of T. cruzi and subsequently treated with 15d-PGJ2 repeatedly for seven days. The inflammatory infiltrate was examined by histologic analysis. Slides were immunohistochemically stained to count the number and the relative size of parasite nests. Infection-induced changes in serum cytokine levels were measured by ELISA. The results demonstrated that treatment with 15d-PGJ2 reduced the inflammatory infiltrate in the skeletal muscle at the site of infection and decreased the number of lymphocytes and neutrophils in the blood. In addition, we found that 15d-PGJ2 led to a decrease in the relative volume density of amastigote nests in cardiac muscle. T. cruzi-infected animals treated with 15d-PGJ2 displayed a statistically significant increase in IL-10 levels with no change in IFN-γ levels. Taken together, we demonstrate that treatment with 15d-PGJ2 in the acute phase of Chagas disease led to a controlled immune response with decreased numbers of amastigote nests, as measured by the volume density

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Section: Discussionmentioning

confidence: 94%

15d-PGJ2 modulates acute immune responses to Trypanosoma cruzi infection

Rodrigues

Miguel

Chica

et al. 2010

Mem. Inst. Oswaldo Cruz

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“…Review of the current human studies as to whether T. cruzi infection leads to hyperglycemia and diabetes on the other hand, is inconclusive. For one, findings of hypoinsulinemia were variable, found in all Chagasic patient groups (Nagajyothi et al 2009; Oliveira et al 1993) or only among a sub-group of infected patients (Guariento et al 1993). In addition, decreased insulin secretion did not consistently correlate with increased prevalence of hyperglycemia.…”

Section: Discussionmentioning

confidence: 99%

Alterations in pancreatic β cell function and Trypanosoma cruzi infection: evidence from human and animal studies

et al. 2016

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The parasite Trypanosoma cruzi causes a persistent infection, Chagas disease, affecting millions of persons in endemic areas of Latin America. As a result of immigration, this disease has now been diagnosed in non-endemic areas worldwide. Although, the heart and gastrointestinal tract are the most studied, the insulin secreting β cell of the endocrine pancreas is also a target of infection. In this review, we summarize available clinical and laboratory evidence to determine whether T. cruzi-infection-mediated changes of β cell function is likely to contribute to the development of hyperglycemia and diabetes. Our literature survey indicates that T. cruzi infection of humans and of experimental animals relates to altered secretory behavior of β cells. The mechanistic basis of these observations appears to be a change in stimulus-secretion pathway function rather than the loss of insulin producing β cells. Whether this attenuated insulin release ultimately contributes to the pathogenesis of diabetes in human Chagas disease however, remains to be determined. Since the etiologies of diabetes are multifactorial including genetic and life-style factors, the use of cell- and animal-based investigations, allowing direct manipulation of these factors, are important tools in testing if reduced insulin secretion has a causal influence on diabetes in the setting of Chagas disease. Long-term clinical investigations will be required to investigate this link in humans.

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“…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).…”

Section: Clinical Formsmentioning

confidence: 99%