title: Differential expression of cytokine genes among sickle-cell-trait (HbAS) and normal (HbAA) children infected with Plasmodium falciparum.
abstract: 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.
authors.affiliation: Central Laboratory, Ministry of Science and Technology, P.O. Box 8076, Khartoum, Sudan.
authors.forename: D A
authors.initials: DA
authors.lastname: Hassan
authors.forename: C
authors.initials: C
authors.lastname: Marques
authors.forename: G M
authors.initials: GM
authors.lastname: Santos-Gomes
authors.forename: V E
authors.initials: VE
authors.lastname: do Rosario
authors.forename: H S
authors.initials: HS
authors.lastname: Mohamed
authors.forename: A M
authors.initials: AM
authors.lastname: Elhussein
authors.forename: M E
authors.initials: ME
authors.lastname: Ibrahim
authors.forename: N H
authors.initials: NH
authors.lastname: Abdulhadi
mesh_terms: D000293:Adolescent; D002648:Child; D002675:Child, Preschool; D003430:Cross-Sectional Studies; D015870:Gene Expression; D006441:Hemoglobin A; D006451:Hemoglobin, Sickle; D006801:Humans; D007113:Immunity, Innate / Q000276:immunology; D007223:Infant; D007371:Interferon-gamma / Q000097:blood / Q000235:genetics*; D007378:Interleukins / Q000097:blood / Q000235:genetics*; D016778:Malaria, Falciparum / Q000097:blood* / Q000276:immunology; D018512:Parasitemia / Q000097:blood / Q000276:immunology; D016133:Polymerase Chain Reaction / Q000379:methods; D012720:Severity of Illness Index; D012805:Sickle Cell Trait / Q000097:blood* / Q000276:immunology; D013223:Statistics as Topic; D013397:Sudan; D014409:Tumor Necrosis Factor-alpha / Q000097:blood / Q000235:genetics*
chemical_list: D006451:Hemoglobin, Sickle; D007378:Interleukins; D014409:Tumor Necrosis Factor-alpha; C028672:hemoglobin AA; C028671:hemoglobin AS; D007371:Interferon-gamma; D006441:Hemoglobin A