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RANTES levels as a determinant of falciparum malaria severity or recovery
Author(s) -
Bujarbaruah D.,
Kalita M. P.,
Baruah V.,
Basumatary T. K.,
Hazarika S.,
Begum R. H.,
Medhi S.,
Bose S.
Publication year - 2017
Publication title -
parasite immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.795
H-Index - 75
eISSN - 1365-3024
pISSN - 0141-9838
DOI - 10.1111/pim.12452
Subject(s) - malaria , immunology , plasmodium falciparum , pathogenesis , biology , cytokine , monocyte , tumor necrosis factor alpha , chemokine , parasite load , inflammation , immune system
Summary The study explored the role of differential RANTES concentrations, its receptor CCR 5 expression and resulting immunomodulation in the pathogenesis and/or recovery from falciparum malaria. The study population included cases of uncomplicated malaria ( UC ‐M, N=128, enrolled on follow‐up basis), severe malaria ( SM , N=25), and healthy controls (N=112). Serum RANTES and TNF ‐α levels were evaluated by ELISA . Monocyte levels and activation profile were studied by flow cytometry. Differential mRNA expression profile was studied by real‐time PCR . Blood parasite count was evaluated by registered pathologists. RANTES concentration was significantly downregulated in SM cases compared to UC ‐M ( P =.046) and controls ( P <.001). Expression of monocyte marker mCD 14, activation markers CCR 5 and CD 40, and downstream effector cytokine TNF ‐α was significantly higher in malaria cases compared to controls, in SM cases compared to UC ‐M. TNF ‐α expression correlated positively with CD 40 and CCR 5 expressions. Follow‐up‐based analysis showed that RANTES concentrations increased on recovery compared to baseline in UC ‐M cases ( P =.106) and inversely correlated with malaria parasite load, mCD 14, CCR 5 and CD 40, and TNF ‐α expressions. These findings suggest an important association of RANTES concentrations in Plasmodium falciparum malaria disease pathogenesis, as well as recovery, mediated through differential modulation and regulated activation of monocytes and cytokine TNF‐α.