The human immune response to Plasmodium falciparum
infection involves the release of
cytokines that may contribute to the control of the parasites' replication. These
cytokines are also involved in the pathogenesis of the
malaria caused by the
infection, leading to the appearance of symptoms of varying severity. In a cross-sectional study, the expression of the genes that code for pro-inflammatory
cytokines (tumour
necrosis factor,
interferon-gamma,
interleukin-6 and
interleukin-12) and anti-inflammatory
cytokines (interleukin-10 and interleukin-4) among 80 children infected with P. falciparum (from a
malaria-endemic area of Sudan) and five healthy controls (from a non-endemic area) was explored. The infected children were either non-sicklers, with severe
malaria (18 children), mild
malaria (30) or no symptoms of
malaria (18), or asymptomatic sicklers (14).
Interleukin-12 was found to be weakly expressed by all the groups of children. In general, compared with the other groups, the asymptomatic non-sicklers had lower expression of all the
cytokines studied. The asymptomatic sicklers had significantly lower expression of tumour
necrosis factor than the non-sicklers with severe
malaria, but these two groups showed similar expression of
interferon-gamma,
interleukin-4 and
interleukin-6. Gene expression of the regulatory
cytokine,
interleukin-10, by the asymptomatic sicklers was significantly lower than that by the non-sicklers with severe
malaria but higher than that recorded in the non-sicklers with mild
malaria. Their regulation of
cytokine release appears to protect sicklers from clinical
malaria.