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Title: Acute Trypanosoma cruzi infection: IL-12, IL-18, TNF, sTNFR and NO in T. rangeli-vaccinated mice. Author: Basso B, Cervetta L, Moretti E, Carlier Y, Truyens C. Journal: Vaccine; 2004 May 07; 22(15-16):1868-72. PubMed ID: 15121297. Abstract: We have developed an experimental model of vaccination against the infection with the protozoa Trypanosoma cruzi, the agent of Chagas disease in Latin America. Vaccination was performed with Trypanosoma rangeli, a non-pathogenic protozoa sharing many antigens with T. cruzi. It strongly protected BALB/c mice, sharply reducing parasitaemia and mortality rate of the acute T. cruzi infection. The aim of the present work was to complete our previous study on the production of IFN-gamma and IL-10 in this vaccination model by investigating the production of IL-12p35 and p40, IL-18, TNF, TNF soluble receptors (sTNFR), and nitric oxide (NO), factors known to play a key role in the outcome of T. cruzi infection. We show that the protection obtained against the acute T. cruzi infection was surprisingly associated with reduced circulating levels of IL-18 and NO, whereas the release of IL-12p40 was enhanced in comparison to non-vaccinated infected animals. IL-12p35 remained undetectable in infected animals, vaccinated or not. The balance between sTNFR and TNF suggested a decrease of TNF bioactivity in vaccinated mice. These results show that the protection induced by the vaccination with T. rangeli against a challenging infection with T. cruzi is not associated with the strong type 1 immune response usually involved in the control of intracellular pathogens, particularly questioning the protective role of NO during the acute phase of T. cruzi infection.[Abstract] [Full Text] [Related] [New Search]