AcuteTrypanosoma cruziinfection: IL-12, IL-18, TNF, sTNFR and NO inT. rangeli-vaccinated mice

• Published in: Vaccine 2004-05, Vol.22 (15-16), p.1868
• Main Authors: Basso, B, Cervetta, L, Moretti, E, Carlier, Y, Truyens, C
• Format: Article
• Language: English
• Subjects: Antigens; Biological activity; Immune response; Infections; Mortality; Nitrates; Nitric oxide; Parasites; Protozoa; Vector-borne diseases
• ISSN: 0264-410X; 1873-2518
• DOI: 10.1016/j.vaccine.2003.11.013

We have developed an experimental model of vaccination against the infection with the protozoaTrypanosoma cruzi, the agent of Chagas disease in Latin America. Vaccination was performed withTrypanosoma rangeli, a non-pathogenic protozoa sharing many antigens withT. cruzi. It strongly protected BALB/c mice, sharply reducing parasitaemia and mortality rate of the acuteT. cruziinfection. The aim of the present work was to complete our previous study on the production of IFN-γ 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 ofT. cruziinfection. We show that the protection obtained against the acuteT. cruziinfection 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 withT. rangeliagainst a challenging infection withT. cruziis 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 ofT. cruziinfection.