BACKGROUND It has been demonstrated that
proteins expressed by
liver-stage
Plasmodium parasites can inhibit the translocation of
transcription factors to the nucleus of different
cells. This process would hinder the expression of immune
genes, such as the
CCL20 chemokine. OBJECTIVE Since CCR6 is the only cognate receptor for CCL20, we investigated the importance of this
chemokine-receptor axis against
rodent malaria.
METHODS CCR6-deficient (KO) and wild-type (WT) C57BL/6
mice were challenged with
Plasmodium berghei (Pb) NK65
sporozoites or infected
red blood cells (iRBCs).
Liver parasitic
cDNA,
parasitemia and
serum cytokine concentrations were respectively evaluated through
reverse transcription-
polymerase chain reaction (RT-PCR),
staining thin-
blood smears with Giemsa
solution, and
enzyme-linked immunosorbent assay (
ELISA). FINDINGS Although the
sporozoite challenges yielded
similar liver parasitic
cDNA and
parasitemia, KO
mice presented a prolonged
survival than WT
mice. After iRBC challenges, KO
mice kept displaying higher
survival rates as well as a decreased
IL-12 p70 concentration in the
serum than WT
mice. CONCLUSION Our data suggest that
malaria triggered by PbNK65
liver- or
blood-stage forms elicit a pro-inflammatory
environment that culminates with a decreased
survival of infected C57BL/6
mice.