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An In vitro Co-infection Model to Study Plasmodium falciparum-HIV-1 Interactions in Human Primary Monocyte-derived Immune Cells
Published on: August 15, 2012
A decrease of plasma macrophage migration inhibitory factor concentration is associated with lower numbers of
Q De Mast1, F C G J Sweep, M McCall
1Department of Internal Medicine, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands. q.demast@aig.umcn.nl
Parasite Immunology
|January 9, 2008
Summary
Plasma macrophage migration inhibitory factor (MIF) levels decrease during early Plasmodium falciparum malaria infection due to a drop in circulating lymphocytes. This finding clarifies contradictory results in previous malaria studies.
Area of Science:
- Immunology
- Infectious Diseases
- Malariology
Background:
- Macrophage migration inhibitory factor (MIF) is implicated in malarial anemia pathogenesis.
- Previous field studies show conflicting results on circulating MIF levels in Plasmodium falciparum malaria.
Purpose of the Study:
- To investigate plasma MIF levels over time during experimental Plasmodium falciparum infection in healthy volunteers.
- To correlate MIF changes with immune cell populations and cytokine profiles.
Main Methods:
- Experimental Plasmodium falciparum infection in 10 healthy volunteers.
- Longitudinal measurement of plasma MIF, lymphocyte counts, monocyte/macrophage counts, IL-10, IL-8, and IL-1beta.
- Controlled study conditions.
Main Results:
- Plasma MIF levels significantly decreased during early blood-stage infection, reaching a nadir at day 8 post-infection.
- A concurrent decrease in circulating lymphocytes, a key MIF source, was observed.
- Monocyte/macrophage counts were unchanged; IL-10 was low, and pro-inflammatory cytokines (IL-8, IL-1beta) were only marginally elevated at MIF nadir.
Conclusions:
- Circulating MIF levels decrease early in blood-stage malaria.
- This reduction is primarily attributed to a decline in circulating lymphocytes.
- The findings help reconcile conflicting reports on MIF in malaria pathogenesis.

