Cell response on malaria vivax thrombocytopenia

Background: Plasmodium vivax emerged as a potentially lethal pathogen and thrombocytopenia is a more common haematological manifestation. Its pathogenesis involves destruction and consumption associated with inflammatory cytokines and structural and functional damage in platelets. Bone marrow disorder is suspected to be associated with thrombocytopenia, and proand anti-inflammatory cytokines may function as serologic markers of thrombocytopenia in vivax malaria. Material and methods: In this study, cellular profiles, chemokines and cytokines of the Th1, Th2 and TH-17 axes were investigated in P. vivax monoinfected patients to evaluate how the cellular response is influenced by thrombocytopenia. Results: Acute malaria led to extended lymphopenia over major lymphocytic subpopulations with increased levels of seven cytokines independent of thrombocytopenia. Platelet count was associated with increased parasitemia, MPV elevation, IL-10 and IL-17 elevation, and retention of CD69+ CD8+ T cells in the peripheral blood. The increase in MPV was independent of parasitemia but associated with retention of lymphocyte subpopulations and decreased levels of inflammatory cytokines. Conclusions: Our findings raised evidence that increased MPV would be a response to thrombocytopenia and balance-dependent pro-inflammatory cytokines reflecting the dynamics of lymphocyte subpopulations in malaria.