Perspectives on Adipose Tissue, Chagas Disease and Implications for the Metabolic Syndrome

The contribution of adipose tissue an autocrine and endocrine organ in the pathogenesis of infectious disease and metabolic syndrome is gaining attention. Adipose tissue and adipocytes are one of the major targets of T. cru...

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Main Authors: Fnu Nagajyothi, Mahalia S. Desruisseaux, Linda A. Jelicks, Fabiana S. Machado, Streamson Chua, Philipp E. Scherer, Herbert B. Tanowitz
Format: Article
Language:English
Published: Wiley 2009-01-01
Series:Interdisciplinary Perspectives on Infectious Diseases
Online Access:http://dx.doi.org/10.1155/2009/824324
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author Fnu Nagajyothi
Mahalia S. Desruisseaux
Linda A. Jelicks
Fabiana S. Machado
Streamson Chua
Philipp E. Scherer
Herbert B. Tanowitz
author_facet Fnu Nagajyothi
Mahalia S. Desruisseaux
Linda A. Jelicks
Fabiana S. Machado
Streamson Chua
Philipp E. Scherer
Herbert B. Tanowitz
author_sort Fnu Nagajyothi
collection DOAJ
description The contribution of adipose tissue an autocrine and endocrine organ in the pathogenesis of infectious disease and metabolic syndrome is gaining attention. Adipose tissue and adipocytes are one of the major targets of T. cruzi infection. Parasites are detected 300 days postinfection in adipose tissue. Infection of adipose tissue and cultured adipocytes triggered local expression of inflammatory mediators resulting in the upregulation of cytokine and chemokine levels. Adipose tissue obtained from infected mice display an increased infiltration of inflammatory cells. Adiponectin, an adipocyte specific protein, which exerts antiinflammatory effects, is reduced during the acute phase of infection. The antiinflammatory regulator peroxisome proliferator activated receptor-γ (PPAR-γ) is downregulated in infected cultured adipocytes and adipose tissue. T. cruzi infection is associated with an upregulation of signaling pathways such as MAPKs, Notch and cyclin D, and reduced caveolin-1 expression. Adiponectin null mice have a cardiomyopathy and thus we speculate that the T. cruzi-induced reduction in adiponectin contributes to the T. cruzi-induced cardiomyopathy. While T. cruzi infection causes hypoglycemia which correlates with mortality, hyperglycemia is associated with increased parasitemia and mortality. The T. cruzi-induced increase in macrophages in adipose tissue taken together with the reduction in adiponectin and the associated cardiomyopathy is reminiscent of the metabolic syndrome.
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spelling doaj-art-f5e19c56648049be8b896d578e9534412025-02-03T05:59:19ZengWileyInterdisciplinary Perspectives on Infectious Diseases1687-708X1687-70982009-01-01200910.1155/2009/824324824324Perspectives on Adipose Tissue, Chagas Disease and Implications for the Metabolic SyndromeFnu Nagajyothi0Mahalia S. Desruisseaux1Linda A. Jelicks2Fabiana S. Machado3Streamson Chua4Philipp E. Scherer5Herbert B. Tanowitz6Department of Pathology, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, NY 10461, USADepartment of Pathology, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, NY 10461, USADepartment of Physiology & Biophysics, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, NY 10461, USADepartment of Biochemistry and Immunology, Institute of Biological Sciences, Federal University of Minas Gerais, Pampula, Belo Horizonte 3127-901, BrazilDepartment of Medicine, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, NY 10461, USATouchstone Diabetes Center, Departments of Internal Medicine and Cell Biology, University of Texas Southwestern, Dallas, TX 75390, USADepartment of Pathology, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, NY 10461, USAThe contribution of adipose tissue an autocrine and endocrine organ in the pathogenesis of infectious disease and metabolic syndrome is gaining attention. Adipose tissue and adipocytes are one of the major targets of T. cruzi infection. Parasites are detected 300 days postinfection in adipose tissue. Infection of adipose tissue and cultured adipocytes triggered local expression of inflammatory mediators resulting in the upregulation of cytokine and chemokine levels. Adipose tissue obtained from infected mice display an increased infiltration of inflammatory cells. Adiponectin, an adipocyte specific protein, which exerts antiinflammatory effects, is reduced during the acute phase of infection. The antiinflammatory regulator peroxisome proliferator activated receptor-γ (PPAR-γ) is downregulated in infected cultured adipocytes and adipose tissue. T. cruzi infection is associated with an upregulation of signaling pathways such as MAPKs, Notch and cyclin D, and reduced caveolin-1 expression. Adiponectin null mice have a cardiomyopathy and thus we speculate that the T. cruzi-induced reduction in adiponectin contributes to the T. cruzi-induced cardiomyopathy. While T. cruzi infection causes hypoglycemia which correlates with mortality, hyperglycemia is associated with increased parasitemia and mortality. The T. cruzi-induced increase in macrophages in adipose tissue taken together with the reduction in adiponectin and the associated cardiomyopathy is reminiscent of the metabolic syndrome.http://dx.doi.org/10.1155/2009/824324
spellingShingle Fnu Nagajyothi
Mahalia S. Desruisseaux
Linda A. Jelicks
Fabiana S. Machado
Streamson Chua
Philipp E. Scherer
Herbert B. Tanowitz
Perspectives on Adipose Tissue, Chagas Disease and Implications for the Metabolic Syndrome
Interdisciplinary Perspectives on Infectious Diseases
title Perspectives on Adipose Tissue, Chagas Disease and Implications for the Metabolic Syndrome
title_full Perspectives on Adipose Tissue, Chagas Disease and Implications for the Metabolic Syndrome
title_fullStr Perspectives on Adipose Tissue, Chagas Disease and Implications for the Metabolic Syndrome
title_full_unstemmed Perspectives on Adipose Tissue, Chagas Disease and Implications for the Metabolic Syndrome
title_short Perspectives on Adipose Tissue, Chagas Disease and Implications for the Metabolic Syndrome
title_sort perspectives on adipose tissue chagas disease and implications for the metabolic syndrome
url http://dx.doi.org/10.1155/2009/824324
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