The liver stage of malaria, caused by the genus Plasmodium, is clinically s
ilent, but immunologically significant. Ample evidence exists for an effect
ive CD8(+) T cell response to this stage as well as the involvement of gamm
a deltaT cells and NK1.1(int) cells in immunized animal models, In contrast
, there is little information concerning responses in a naive host. Here we
report that several host gene expressions in the liver, spleen, and kidney
of BALB/c mice are altered during the liver stage of Plasmodium yoelii inf
ection. Really interesting new gene 3 (Ring3), semaphorin subclass 4 member
G, glutamylcysteine synthetase, and p45 NF erythroid 2 were all up-regulat
ed 24 h after infection with P. yoelii. Semaphorin subclass 4 member G expr
ession was elevated in the kidney, whereas Ring3 was elevated in both splee
n and kidney. The expression of TNF-alpha (TNF-alpha and IFN-gamma) were do
wn-regulated in all three tissues tested except in infected spleen where IF
N-gamma was elevated, P. yoelii-related host gene changes were compared wit
h those in Toxoplasma gondii-infected livers. Ring3 expression increased 5-
fold over control values, whereas expression of the other transcripts remai
ned unchanged. TNF-alpha and IFN-gamma expressions were increased in the To
xoplasma-infected livers. The uniform increase of Ring3 expression in both
Plasmodium- and Toxoplasma-infected livers suggests an innate immune respon
se against parasitic infections, whereas the other gene expression changes
are consistent with Plasmodium parasite-specific responses. Taken together,
these changes suggest the immune responses to P. yoelii infection are both
parasite and organ specific.