To find out
host gene expression profiles after malarial infection.<
h4 id="absSec_2">Met
hodsh4>
Further time-course microarray analysis of peripheral blood mononuclear cells focusing on malaria pathogenesis was performed.
<
h4 id="absSec_3">Resultsh4>
Up-regulation of coagulation-related genes, heat shock proteins, glycolytic enzymes, glucose transporters, and vacuolar H+-ATPases was found in acute febrile malaria. In early malaria, prior to detectable parasitemia, CD36 and ICAM1 were up-regulated. During acute malaria, there is correlation between IL-1β and heat shock proteins. CD163, a hemoglobin scavenger receptor, was up-regulated in acute malaria to potentially facilitate free hemoglobin up-take by leukocytes. In acute malaria, high MafB gene expression was negatively correlated with hemoglobin and platelet counts. Consistent with hemoglobin down-regulation, peripheral red blood cell counts tended to increase during acute malaria. Up-regulations of red blood cell and leukocyte binding mediators like CD36, ICAM1, thrombospondin, and thrombomodulin may contribute to the pathogenesis of cerebral malaria. Similarly, up-regulation of correlated glycolytic enzymes, glucose transporter and H+-ATPases may contribute to the hypoglycemia and metabolic acidosis frequently observed in serious malaria patients. Overall gender effects on gene expression profiles between male and female were not apparent, except for some hemoglobins were significantly down-regulated in male versus female, which suggesting males are prone to malaria-related anemia.
<
h4 id="absSec_4">Conclusionsh4>
Leukocyte gene expression profiles can explain the pathogenesis of malarial complication such as fever, metabolic acidosis, hypoglycemia, anemia, and coagulopathy.
