Inducible Nitric Oxide Synthase and Arginase Expression in Heart Tissue during Acute Trypanosoma cruzi Infection in Mice: Arginase I Is Expressed in Infiltrating CD68+ Macrophages

In Chagas disease, which is caused by Trypanosoma cruzi, macrophages and cardiomyocytes are the main targets of infection. Classical activation of macrophages during infection is protective, whereas alternative activation of macrophages is involved in the survival of host cells and parasites. We stu...

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Bibliographic Details
Published in:The Journal of infectious diseases 2008-06, Vol.197 (12), p.1772-1782
Main Authors: Cuervo, Henar, Pineda, Miguel A., Aoki, M. Pilar, Gea, Susana, Fresno, Manuel, Gironès, Núria
Format: Article
Language:English
Subjects:
Acute Disease
Animals
Antibodies
Antigens, CD - metabolism
Antigens, Differentiation, Myelomonocytic - metabolism
Arginase - genetics
Arginase - metabolism
Biological and medical sciences
Carrier Proteins
Chagas Disease - enzymology
Cytokines
Cytokines - metabolism
Enzyme Activation
Fundamental and applied biological sciences. Psychology
Gene Expression Regulation, Enzymologic
Heart
Human protozoal diseases
Inductive reasoning
Infections
Infectious diseases
Intramolecular Oxidoreductases - metabolism
Macrophages
Macrophages - enzymology
Macrophages - immunology
Medical sciences
Messenger RNA
Mice
Mice, Inbred BALB C
Mice, Inbred C57BL
Microbiology
Myocardium
Myocardium - cytology
Myocardium - enzymology
Myocardium - immunology
Myocytes, Cardiac - metabolism
Nitric Oxide Synthase Type II - genetics
Nitric Oxide Synthase Type II - metabolism
Oxides
Parasites
Parasitic diseases
Prostaglandin-E Synthases
Protozoal diseases
Specific Pathogen-Free Organisms
Trypanosoma cruzi
Trypanosomiasis
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Summary:In Chagas disease, which is caused by Trypanosoma cruzi, macrophages and cardiomyocytes are the main targets of infection. Classical activation of macrophages during infection is protective, whereas alternative activation of macrophages is involved in the survival of host cells and parasites. We studied the expression of inducible nitric oxide synthase (iNOS) and arginase as markers of classical and alternative activation, respectively, in heart tissue during in vivo infection of BALB/c and C57BL/6 mice. We found that expression of arginase I and II, as well as that of ornithine decarboxylase, was much higher in BALB/c mice than in C57BL/6 mice and that it was associated with the parasite burden in heart tissue. iNOS and arginase II were expressed by cardiomyocytes. Interestingly, heart-infiltrated CD68+ macrophages were the major cell type expressing arginase I. T helper (Th) 1 and Th2 cytokines were expressed in heart tissue in both infected mouse strains; however, at the peak of parasite infection, the balance between Th1 and Th2 predominantly favored Th1 in C57BL/6 mice and Th2 in BALB/c mice. The results of the present study suggest that Th2 cytokines induce arginase expression, which may influence host and parasite cell survival but which might also down-regulate the counterproductive effects triggered by iNOS in the heart during infection.
ISSN:0022-1899
1537-6613
DOI:10.1086/529527