AIMS: To monitor the expression of intercellular adhesion molecule I (ICAM-I) in vitro after stimulation of human macrophages with Plasmodium falciparum antigens, as well as the plasma concentrations of soluble ICAM-I (SICAM-I) in vivo in malarial patients. METHODS: Human mononuclear leucocytes were cultured and stimulated for four hours with 300 ng/ml exogenous P falciparum antigens. CD14 and CD54 (ICAM-I) expression was monitored using flow cytometry. Soluble ICAM-I (s ICAM-I) was also measured in the blood of 122 outpatients with malaria before and after treatment (Rio Branco, Acre, Brazil). RESULTS: ICAM-I expression increased from 15% to 375% after four hours of stimulation. When sICAM-I was analysed in the plasma of 122 patients with P falciparum or Plasmodium vivax malaria by enzyme immunoassay, significant increases were found. These were more pronounced in patients with P falciparum malaria, compared with healthy controls, and with the same patients four weeks after treatment. CONCLUSION: ICAM-I expression may also be upregulated in human macrophages by exogenous Plasmodium antigens as well as by cytokines during the acute phase of malaria. sICAM-I concentrations are downregulated after treatment, probably caused by the absence of circulating Plasmodium antigens.
AIMS: To monitor the expression of intercellular adhesion molecule I (ICAM-I) in vitro after stimulation of human macrophages with Plasmodium falciparum antigens, as well as the plasma concentrations of soluble ICAM-I (SICAM-I) in vivo in malarialpatients. METHODS:Human mononuclear leucocytes were cultured and stimulated for four hours with 300 ng/ml exogenous P falciparum antigens. CD14 and CD54 (ICAM-I) expression was monitored using flow cytometry. Soluble ICAM-I (s ICAM-I) was also measured in the blood of 122 outpatients with malaria before and after treatment (Rio Branco, Acre, Brazil). RESULTS: ICAM-I expression increased from 15% to 375% after four hours of stimulation. When sICAM-I was analysed in the plasma of 122 patients with P falciparum or Plasmodium vivaxmalaria by enzyme immunoassay, significant increases were found. These were more pronounced in patients with P falciparum malaria, compared with healthy controls, and with the same patients four weeks after treatment. CONCLUSION: ICAM-I expression may also be upregulated in human macrophages by exogenous Plasmodium antigens as well as by cytokines during the acute phase of malaria. sICAM-I concentrations are downregulated after treatment, probably caused by the absence of circulating Plasmodium antigens.
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