| Sumario: | Tumor necrosis factor-α (TNF-α) plays a role in the host's defence against infections with African trypanosomes. It helps to control the blood stream form of the parasite and in <em>Trypanosoma congolense</em> infections, it also prolongs survival. The mechanisms by which this cytokine can influence parasitemia and survival are unknown. Therefore, the levels of acute phase proteins and other inflammatory cytokines were monitored in trypano-tolerant wild-type and TNF-α-deficient mice during a <em>T. congolense</em> infection.
The titres of ceruloplasmin (CP), α1-acid glycoprotein (AGP) and serum amyloid P (SAP) increased and reached their peaks at 11 days post-infection, when the first peak of parasitemia was observed. No significant differences were observed in the acute phase protein profiles between the two mouse strains. Also the profiles of serum titres of IFN-γ, IL-1α, IL-6 and IL-10 were not significantly different. Our present results indicate that acute phase protein and cytokine responses can be induced in the absence of TNF-α during a <em>T. congolense</em> infection in mice, and that the susceptibility of the TNF-α-deficient mice is not due to modulation of expression of these molecules.
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