An immuno-inflammatory profiling of asymptomatic individuals in a malaria endemic area in Uganda.

Malaria caused by Plasmodium falciparum leads to the destruction of red blood cells (RBCs). A better understanding of how naturally immune individuals control infections should be valuable for future vaccine studies. Antibodies against RBCs and RBC surface antigens were measured together with different inflammatory markers in healthy adults living in a malaria endemic area of Uganda and compared to Swedish healthy adults. Antibodies binding to RBCs were clearly elevated in Ugandans compared to Swedish samples, and for RBC surface antigens the Ugandans had higher levels of antibodies against JMH, but not against Cromer or Kell. Twenty-eight percent of the Ugandans were PCR-positive for P. falciparum, and these had higher levels of IgG against parasite extract and more inhibition in functional growth/invasion assays, but levels of antibodies against RBC, RBC surface antigens, results from Direct Antiglobulin Tests (DAT) and indirect antiglobulin tests were similar when compared with PCR-negative individuals. When inflammatory markers (α-1-antitrypsin, haptoglobin, orosomucoid/α-1-acid glycoprotein, CRP, IgG, IgA and IgM) were measured there were in general almost no signs of inflammation except for clearly elevated levels of IgG. Some had low levels of haptoglobin and for orosomucoid more than half of the individuals had clearly reduced levels. There was no correlation between the inflammatory markers and PCR-positivity, antibodies against RBCs or parasites. In conclusion, for healthy adults living in a malaria endemic area, there was a clear presence of antibodies against RBCs in parallel with high levels of IgG and almost no signs of inflammation, even though many individuals were carrying parasites.