Soluble products of inflammatory reactions are not induced in children with asymptomatic Plasmodium falciparum infections

A proportion of children with Plasmodium falciparum infection have a high parasitaemia without accompanying fever, indicative of different clinical thresholds of parasitaemia. Higher levels of IL‐10, IL‐1Ra and sIL‐4R but not sIL‐2R were found in children with P. falciparum malaria, compared with levels in children with asymptomatic P. falciparum infections and in healthy children. Concentrations of IL‐10 and IL‐1Ra were correlated with levels of parasitaemia, but the association of cytokine levels with disease was independent of the association with parasitaemia. Children may tolerate a high parasitaemia by neutralizing the parasite‐derived toxins. When studying potential anti‐toxic molecules we found that children with symptomatic infections had lower concentrations of a phospholipid‐binding molecule, β2‐glycoprotein I (β2‐GPI), compared with children with asymptomatic infections or healthy children. In conclusion, cytokines were found in much higher concentrations in children with symptomatic P. falciparum malaria than in children with asymptomatic infections, whilst the former had lower concentrations of β2‐GPI.

[1]  J. Taverne,et al.  Malaria: toxins, cytokines and disease , 1995, Parasite immunology.

[2]  B. Greenwood,et al.  Increased concentrations of interleukin-6 and interleukin-1 receptor antagonist and decreased concentrations of beta-2-glycoprotein I in Gambian children with cerebral malaria , 1994, Infection and immunity.

[3]  D. Kwiatkowski,et al.  Inhibitory immunoglobulin M antibodies to tumor necrosis factor-inducing toxins in patients with malaria , 1994, Infection and immunity.

[4]  C. Facer,et al.  High levels of anti‐phospholipid antibodies in uncomplicated and severe Plasmodium falciparum and in P. vivax malaria , 1994, Clinical and experimental immunology.

[5]  J. Banchereau,et al.  High levels of circulating IL‐10 in human malaria , 1994, Clinical and experimental immunology.

[6]  D. Kwiatkowski,et al.  Plasmodium falciparum varies in its ability to induce tumor necrosis factor , 1993, Infection and immunity.

[7]  T. Theander,et al.  Anti-phospholipid antibodies in patients with Plasmodium falciparum malaria. , 1993, Immunology.

[8]  K. Marsh,et al.  Malaria-a neglected disease? , 1992, Parasitology.

[9]  J. Playfair,et al.  Antibodies against phosphatidylinositol and inositol monophosphate specifically inhibit tumour necrosis factor induction by malaria exoantigens. , 1992, Immunology.

[10]  J. Playfair,et al.  Detoxified exoantigens and phosphatidylinositol derivatives inhibit tumor necrosis factor induction by malarial exoantigens , 1992, Infection and immunity.

[11]  J. Playfair,et al.  Malarial parasites induce TNF production by macrophages. , 1988, Immunology.

[12]  I. Schousboe Addition of deoxycholate in electroimmunoassay and crossed immunofocusing for quantification of beta 2-glycoprotein I and its subfractions. , 1982, Journal of biochemical and biophysical methods.

[13]  D. Kwiatkowski,et al.  Variation in the TNF-alpha promoter region associated with susceptibility to cerebral malaria. , 1994, Nature.

[14]  B. Greenwood,et al.  Comparison of two simple methods for determining malaria parasite density. , 1991, Transactions of the Royal Society of Tropical Medicine and Hygiene.

[15]  R. Snow,et al.  Why do some African children develop severe malaria? , 1991, Parasitology today.

[16]  J. Playfair,et al.  The malaria vaccine: anti-parasite or anti-disease? , 1990, Immunology today.

[17]  D. Kwiatkowski,et al.  Tumour necrosis factor production in Falciparum malaria and its association with schizont rupture. , 1989, Clinical and experimental immunology.