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Antibodies Alters Trypanosome-Susceptible Mice to a Resistant-Like Phenotype1
Department of Veterinary Microbiology, Western College of Veterinary Medicine, University of Saskatchewan, Saskatoon, Canada
The mechanisms regulating resistance or susceptibility to African
trypanosomes have been enigmatic. In this study, we assessed the
production of several cytokines (IL-4, IFN-
, and TNF-
) in vivo
and in vitro using genetically susceptible (BALB/c) or resistant
(C57BL/6) mice infected with cloned Trypanosoma
congolense and the role of these cytokines in pathogenesis of
this infection. Plasma of infected BALB/c mice contained higher levels
of IL-4 and IFN- than the plasma of infected C57BL/6 mice.
Conversely, plasma TNF- levels were elevated significantly in the
resistant mice relative to the susceptible ones. Splenic IFN- mRNA
appeared earlier and were maintained at higher levels in infected
BALB/c than in C57BL/6 mice. Both spontaneous and Con A-induced
secretions of IL-4 and IFN- by splenocytes from infected BALB/c mice
were significantly higher than those from their C57BL/6 counterparts.
Con A-induced proliferation of splenocytes from infected BALB/c mice
was progressively suppressed. Nitric oxide was not involved in this
suppression, but the suppression was positively correlated with IFN-
secretion. Addition of neutralizing Abs to IFN- to cultures of Con
A-stimulated spleen cells from infected BALB/c mice effectively
reversed this suppression. Furthermore, administration of
anti-IFN- Abs to BALB/c mice early during infection dramatically
shifted the phenotype of these susceptible mice to a more
resistant-like phenotype, as expressed by a low and undulating
parasitemia and a >300% increase in survival period. These results
strongly suggest that the enhanced induction and secretion of IFN-
during T. congolense infections contribute to the
relative susceptibility of BALB/c mice to the
disease.
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