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McGill University Centre for the Study of Host Resistance, and Montreal General Hospital Research Institute, Montreal, Quebec, Canada
As previously reported, blood-stage Plasmodium
chabaudi AS malaria is lethal by days 10–12 postinfection in
susceptible A/J mice that mount an early, predominantly Th2 response.
In contrast, resistant C57BL/6 (B6) mice clear the infection by 4 wk
with an early Th1 response. In this study, we analyzed in vivo
production of IL-12, a potent Th1-inducing cytokine, during the first 5
days after P. chabaudi AS infection in these mice. By
day 2, serum IL-12 p70 levels were significantly increased in B6 mice
over basal levels and were also significantly higher compared with A/J
mice that showed no significant changes in serum p70 levels after
infection. Splenectomy of resistant B6 mice before infection
demonstrated that the spleen is the major source of systemic IL-12 in
these hosts. Splenic mRNA levels of both p40 and p35 were significantly
higher in A/J mice; however, the ratios of p40/p35 mRNA levels were
similarly up-regulated in both strains. Furthermore, B6 but not A/J
mice showed significant up-regulation of splenic IL-12R ß2 mRNA over
basal levels by days 3 and 4, coincident with sustained up-regulation
of splenic IFN-
mRNA levels on days 3–5. However, IL-12R ß1 mRNA
levels in the spleen were similarly up-regulated in both mouse strains
by day 3. Taken together, these data suggest that high systemic IL-12
production, accompanied by an early and sustained up-regulation of both
IL-12R ß1 and ß2 mRNA levels in the spleen, as occurs in resistant
B6 mice, appears to preferentially induce protective Th1 responses
against blood-stage malaria.
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