Sequential Changes of the Connective Matrix Components of the Myocardium (Fibronectin and Laminin) and Evolution of Cardiac Fibrosis in Mice Infected with Trypanosoma cruzi

Andrade, Sônia Gumes; Ja, Grimaud; Stocker-Guerret, Sylviane

doi:10.4269/ajtmh.1989.40.252

Cited by 41 publications

(33 citation statements)

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“…CCC [2,8]) are downregulated during the late stages of the infection. In addition, integrin signaling-associated genes were also affected, including LIMS1, NEDD9, CYR61, and ITGA5, which were downregulated.…”

Section: Resultsmentioning

confidence: 99%

Trypanosoma cruzi Infection Induces a Global Host Cell Response in Cardiomyocytes

et al. 2011

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Chagas' disease, caused by the hemoflagellate protozoan Trypanosoma cruzi, affects millions of people in South and Central America. Chronic chagasic cardiomyopathy, the most devastating manifestation of this disease, occurs in approximately one-third of infected individuals. Events associated with the parasite's tropism for and invasion of cardiomyocytes have been the focus of intense investigation in recent years. In the present study, we use murine microarrays to investigate the cellular response caused by invasion of primary murine cardiomyocytes by T. cruzi trypomastigotes. These studies identified 353 murine genes that were differentially expressed during the early stages of invasion and infection of these cells. Genes associated with the immune response, inflammation, cytoskeleton organization, cell-cell and cell-matrix interactions, apoptosis, cell cycle, and oxidative stress are among those affected during the infection. Our data indicate that T. cruzi induces broad modulations of the host cell machinery in ways that provide insight into how the parasite survives, replicates, and persists in the infected host and ultimately defines the clinical outcome of the infection.

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Section: Resultsmentioning

confidence: 99%

Trypanosoma cruzi Infection Induces a Global Host Cell Response in Cardiomyocytes

et al. 2011

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“…More recently, it was shown that, compared with dilated cardiomyopathy, chronic chagasic myocarditis presents a distinctive pattern of ECM abnormalities (19). Increased expression of ECM components including FN, LN and types III and IV collagen, and remodeling of matrix components associated with the progression of inflammation have also been detected in the heart tissue of T. cruzi-infected mice (20). However, focal connective tissue damage with multiple areas devoid of ECM components was observed in inflamed atria of early acutely infected mice (21).…”

Section: The Host Answersmentioning

confidence: 99%

Trypanosoma cruzi infection: a continuous invader-host cell cross talk with participation of extracellular matrix and adhesion and chemoattractant molecules

Marino¹,

Silva²,

Pinho

et al. 2003

Braz J Med Biol Res

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Several lines of evidence have shown that Trypanosoma cruzi interacts with host extracellular matrix (ECM) components producing breakdown products that play an important role in parasite mobilization and infectivity. Parasite-released antigens also modulate ECM expression that could participate in cell-cell and/or cell-parasite interactions. Increased expression of ECM components has been described in the cardiac tissue of chronic chagasic patients and diverse target tissues including heart, thymus, central nervous system and skeletal muscle of experimentally T. cruzi-infected mice. ECM components may adsorb parasite antigens and cytokines that could contribute to the establishment and perpetuation of inflammation. Furthermore, T. cruzi-infected mammalian cells produce cytokines and chemokines that not only participate in the control of parasitism but also contribute to the establishment of chronic inflammatory lesions in several target tissues and most frequently lead to severe myocarditis. T. cruzi-driven cytokines and chemokines may also modulate VCAM-1 and ICAM-1 adhesion molecules on endothelial cells of target tissues and play a key role in cell recruitment, especially of activated VLA-4 + LFA-1 + CD8 + T lymphocytes, resulting in a predominance of this cell population in the inflamed heart, central nervous system and skeletal muscle. The VLA-4 + -invading cells are surrounded by a fine network of fibronectin that could contribute to cell anchorage, activation and effector functions. Since persistent "danger signals" triggered by the parasite and its antigens are required for the establishment of inflammation and ECM alterations, therapeutic interventions that control parasitism and selectively modulate cell migration improve ECM abnormalities, paving the way for the development of new therapeutic strategies improving the prognosis of T. cruzi-infected individuals.

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“…The requirement and functional participation of L-selectin (CD62L), leukocyte function-associated antigen 1 (LFA-1; CD11a,CD18) and very late activation antigen 4 (VLA-4; CD49d,CD29; α4β1) in T cell activation and migration has been extensively demonstrated in other models (Springer 1995, Sprent et al 1997 (Laucella et al 2001). Increased expression of ECM components particularly fibronectin (FN), a VLA-4 ligand, have been previously detected in the myocardium of T. cruziinfected mice during the acute and chronic phases (Andrade et al 1989). Studying Colombiana-infected C3H/ HeJ mice, we confirmed this finding and showed that a fine interstitial FN mesh present in the inflamed heart involves VLA-4 + CD4 + and CD8 + T cells (dos Santos et al 2001) as well as the infected and non-infected myocytes (E Roffê & J Lannes-Vieira, unpublished observations).…”

mentioning

confidence: 99%

Trypanosoma cruzi-elicited CD8+ T cell-mediated myocarditis: chemokine receptors and adhesion molecules as potential therapeutic targets to control chronic inflammation?

Lannes-Vieira

2003

Mem. Inst. Oswaldo Cruz

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Sequential Changes of the Connective Matrix Components of the Myocardium (Fibronectin and Laminin) and Evolution of Cardiac Fibrosis in Mice Infected with Trypanosoma cruzi

Cited by 41 publications

References 0 publications

Trypanosoma cruzi Infection Induces a Global Host Cell Response in Cardiomyocytes

Trypanosoma cruzi Infection Induces a Global Host Cell Response in Cardiomyocytes

Trypanosoma cruzi infection: a continuous invader-host cell cross talk with participation of extracellular matrix and adhesion and chemoattractant molecules

Trypanosoma cruzi-elicited CD8+ T cell-mediated myocarditis: chemokine receptors and adhesion molecules as potential therapeutic targets to control chronic inflammation?

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