Physica A 388 (2009) 1747–1754 Contents lists available at ScienceDirect Physica A journal homepage: www.elsevier.com/locate/physa Modeling the Chagas’ disease after stem cell transplantation Viviane Galvão a,* , José Garcia Vivas Miranda b a Departamento de Ciências Biológicas, Universidade Estadual de Feira de Santana, 44036-900, Feira de Santana – BA, Brazil b Departamento de Física da Terra e do Meio Ambiente, Instituto de Física, Universidade Federal da Bahia, 40210-340, Salvador – BA, Brazil article info Article history: Received 7 October 2008 Received in revised form 6 January 2009 Available online 17 January 2009 Keywords: Computational model Chronic chagasic cardiomyopathy Autonomous agent Cellular therapy abstract A recent model for Chagas’ disease after stem cell transplantation is extended for a three- dimensional multi-agent-based model. The computational model includes six different types of autonomous agents: inflammatory cell, fibrosis, cardiomyocyte, proinflammatory cytokine tumor necrosis factor-α, Trypanosoma cruzi, and bone marrow stem cell. Only fibrosis is fixed and the other types of agents can move randomly through the empty spaces using the three-dimensional Moore neighborhood. Bone marrow stem cells can promote apoptosis in inflammatory cells, fibrosis regression and can differentiate in cardiomyocyte. T. cruzi can increase the number of inflammatory cells. Inflammatory cells and tumor necrosis factor-α can increase the quantity of fibrosis. Our results were compared with experimental data giving a fairly fit and they suggest that the inflammatory cells are important for the development of fibrosis. © 2009 Elsevier B.V. All rights reserved. 1. Introduction The discovery of the pluripotency of adult bone marrow stem cells has opened new perspectives for the treatment of patients with chronic chagasic cardiomyopathy. This disease is caused by the hemoflagellate parasite Trypanosoma cruzi and one of the leading causes of heart failure in Latin America. Chagas’ disease is transmitted by an insect of the subfamily Triatominae, or by blood transfusion. Most of the T. cruzi-infected individuals remain asymptomatic. This subclinical state is called the indeterminate form of Chagas’ disease. However, around 30% of the T. cruzi-infected individuals develop a cardiac complication, in a late phase of the disease. Chronic chagasic cardiomyopathy is characterized by a diffuse inflammatory reaction and a severe fibrosis [1–4]. In the chronic phase of the disease, the presence of T. cruzi is associated with chronic inflammatory response [2]. The elevated production of the proinflammatory cytokine tumor necrosis factor-α (TNF- α) causes the fibrosis growth [4]. The regenerative potential of bone marrow stem cell transplantation has been under investigation in experimental models of ischemic cardiomyopathy and chronic chagasic cardiomyopathy [4,5]. A stem cell is a particular type of cell that can renew itself and possesses ability to divide in many different types of specialized cells [5–7]. Experimental evidences have shown that the transplant of bone marrow stem cell can promote apoptosis in non-normal cells and can differentiate into a normal cell of the tissue [5]. An experimental model to describe the effects of adult bone marrow transplant in the chronic chagasic cardiomyopathy was developed by Soares et al. [4]. In this model, bone marrow cells were injected into chronic chagasic mice leading to a considerable reduction in the number of inflammatory cells and in the fibrosis area. The authors suggest that bone marrow stem cells can promote apoptosis of inflammatory cells and fibrosis regression. The scientific contribution in computational models for parasites includes interaction between T. cruzi and antibodies during the acute phase of Chagas infection [8,9], competitive parasite–antibody interaction in the intracellular and * Corresponding author. Tel.: +55 75 3224 8132; fax: +55 75 3224 8132. E-mail address: vivianegalvao@uefs.br (V. Galvão). 0378-4371/$ – see front matter © 2009 Elsevier B.V. All rights reserved. doi:10.1016/j.physa.2009.01.012