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*
Department of Allergology, Institute of Medical Science, The University of Tokyo, Tokyo, Japan; and
Gunma Prefectural College of Health Sciences, Maebashi, Japan
We studied whether the infection with a blood-stage murine malaria
lethal Plasmodium berghei NK65 induces IL-12
production, and if so, how the IL-12 production is involved in the
protection or pathogenesis. The infection of C57BL/6 mice enhanced mRNA
expression of IL-12 p40 and also IFN-
, IL-4, and IL-10 in both
spleen and liver during the early course of the infection. It also
enhanced the mRNA expression of TNF-
, Fas ligand, and
cytokine-inducible nitric oxide synthase. Increased IL-12 p40
production was also observed in the culture supernatant of spleen cells
and in sera of infected mice. In addition, the infection caused massive
liver injury with elevated serum glutamic-oxaloacetic transaminase and
serum glutamic-pyruvic transaminase activities and body weight loss.
Treatment of these infected mice with neutralizing mAb against IL-12
prolonged the survival and diminished the liver injury with reduced
elevation of serum serum glutamic-oxaloacetic transaminase and serum
glutamic-pyruvic transaminase activities and decreased body weight
loss. However, the anti-IL-12 treatment did not affect parasitemia,
and all these mice eventually died. Similar results were obtained when
infected mice were treated with neutralizing mAb against IFN-.
Moreover, anti-IL-12 treatment greatly reduced the secretion and
mRNA expression of IFN- in both spleen and liver. These results
suggest that the lethal P. berghei NK65 infection induces
IL-12 production and that the IL-12 is involved in the pathogenesis of
liver injury via IFN- production rather than the protection.
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