Short treatment with the tumour necrosis factor-α blocker infliximab diminishes chronic chagasic myocarditis in rats without evidence of Trypanosoma cruzi reactivation
Autor: | Silvia Revelli, Oscar Bottasso, Ana Lía Nocito, Germán H. Fontanella, Ana Rosa Pérez |
---|---|
Rok vydání: | 2009 |
Předmět: |
Chagas Cardiomyopathy
Male Necrosis Myocarditis Translational Studies Trypanosoma cruzi medicine.medical_treatment Immunology Antibodies Protozoan Parasitemia Pathogenesis Random Allocation medicine Animals Immunology and Allergy RNA Messenger biology Reverse Transcriptase Polymerase Chain Reaction Tumor Necrosis Factor-alpha business.industry Antibodies Monoclonal Interleukin Heart DNA Protozoan medicine.disease biology.organism_classification Immunohistochemistry Infliximab Rats Cytokine Models Animal Tumor necrosis factor alpha medicine.symptom business Immunosuppressive Agents medicine.drug |
Zdroj: | Clinical and Experimental Immunology. 157:291-299 |
ISSN: | 1365-2249 0009-9104 |
DOI: | 10.1111/j.1365-2249.2009.03946.x |
Popis: | Summary Tumour necrosis factor (TNF)-α is crucial for resistance to Trypanosoma cruzi acute infection, but there is scant information on its role during the chronic phase. To address this issue, we analysed whether a short treatment with a TNF-α blocker affected the course and characteristics of chronic disease in a rat experimental model of T. cruzi infection. An anti-TNF-α agent (infliximab) was administered during the chronic phase for a period of 4 weeks (3 mg/kg/week), while control infected rats were inoculated with saline physiological solution. Search for parasites yielded non-successful results in all infected groups, irrespective of treatment. Nevertheless, the presence of T. cruzi kDNA in heart tissue was detected in infected and infected plus treated animals. Because infliximab might induce changes in the anti-parasite cytokine response, circulating levels of interleukin (IL)-10, interferon-gamma and nitric oxide were evaluated. An increase in IL-10 levels was observed only in the infected group treated with the anti-TNF-α blocker compared to the remaining groups (P |
Databáze: | OpenAIRE |
Externí odkaz: |