Modulation of Chagasic Cardiomyopathy by Interleukin-4 : Dissociation between Inflammation and Tissue Parasitism

• Published in: The American journal of pathology Vol. 159; no. 2; pp. 703 - 709
• Main Authors: Soares, Milena B. P, Silva-Mota, Katia N, Lima, Ricardo S, Bellintani, Moema C, Pontes-de-Carvalho, Lain, Ribeiro-dos-Santos, Ricardo
• Format: Journal Article
• Language: English
• Published: Bethesda, MD ASIP 01.08.2001; American Society for Investigative Pathology
• Subjects: Animals; Biological and medical sciences; Chagas Cardiomyopathy - genetics; Chagas Cardiomyopathy - immunology; Chagas Cardiomyopathy - pathology; Experimental protozoal diseases and models; Immunity, Innate - genetics; Immunity, Innate - immunology; Infectious diseases; Inflammation - immunology; Inflammation - pathology; Interleukin-4 - deficiency; Interleukin-4 - genetics; Interleukin-4 - physiology; Lymphocyte Activation; Medical sciences; Mice; Mice, Inbred BALB C; Mice, Knockout; Mice, Nude; Myocarditis - genetics; Myocarditis - immunology; Myocarditis - pathology; Parasitemia - immunology; Parasitemia - pathology; Parasitic diseases; Protozoal diseases; Regular; T-Lymphocytes, Helper-Inducer - immunology; Time Factors; Trypanosoma cruzi; Immunohistochemistry; Protozoal disease; Cardiomyopathy; Cytokine; Rodentia; Th1 lymphocyte; Chagas disease; Cardiovascular disease; Inflammation; Parasitosis; Myocardial disease; Infection; Pathology; Vertebrata; Interleukin 4; Experimental disease; Mammalia; Mouse; Heart disease; Animal; Trypanosomiasis
• ISSN: 0002-9440; 1525-2191
• DOI: 10.1016/S0002-9440(10)61741-5

Chronic chagasic cardiomyopathy (CChC) is characterized by an inflammatory reaction which may eventually lead to heart enlargement, arrythmia, and death. As described herein, interleukin-4-deficient mice mount increased specific T helper (Th) 1 immune responses when infected with Trypanosoma cruzi, as compared to wild-type mice. Interestingly, these mice had reduced parasitism and mortality and exacerbated inflammation in their hearts, demonstrating a clear dissociation between inflammation and parasite load. The modulation of these phenomena so as to maximize host and parasite survivals may depend on a fine balance between Th responses, in which a Th1 response will, on one hand, control parasitism and, on the other hand, enhance heart inflammation throughout the course of the infection.