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|Title:||Activation of nuclear factor kappa B in peripheral blood mononuclear cells from malaria patients|
Mahidol University. Faculty of Tropical Medicine. Department of Tropical Pathology
Mahidol University. Faculty of Tropical Medicine. Department of Tropical Hygiene
Mahidol University. Faculty of Tropical Medicine. Department of Clinical Tropical Medicine
Mahidol University. Faculty of Science. Department of Pathobiology.
|Keywords:||Malaria;Plasmodium falciparum;Plasmodium vivax;Nuclear factor kappa B;Peripheral blood mononuclear cells;Interleukin-10;Tumor necrosis factor;Open Access article|
|Citation:||Punsawad C, Krudsood S, Maneerat Y, Chaisri U, Tangpukdee N, Pongponratn E. et al. Activation of nuclear factor kappa B in peripheral blood mononuclear cells from malaria patients. Malar J. 2012 Jun 10;11:191.|
|Abstract:||BACKGROUND: Malaria parasites and their products can activate a specific immune response by stimulating cytokine production in the host's immune cells. Transcription nuclear factor kappa B (NF-κB) is an important regulator for the control of many pro-inflammatory genes, such as interleukin-1 (IL-1) and tumor necrosis factor (TNF). The activation and expression of NF-κB p65 in peripheral blood mononuclear cells (PBMCs) of malaria patients were investigated and correlated with the levels of IL-10 and TNF to study the nature of NF-κB p65 and its linkage to inflammatory cytokines. METHODS: The sample group comprised 33 patients admitted with malaria caused by Plasmodium vivax (n = 11), uncomplicated Plasmodium falciparum (n = 11), and complicated Plasmodium falciparum (n = 11). Peripheral blood was collected at admission and on day 7 for PBMC isolation. Healthy subjects were used as a control group. The expressions of NF-κB p65 in the PBMCs from malaria patients and the plasma levels of IL-10 and TNF were measured by using enzyme-linked immunosorbent assay (ELISA). The immunofluorescence technique was used to determine NF-κB nuclear translocation. RESULTS: At admission, patients with P. vivax and uncomplicated P. falciparum had significantly elevated phospho-NF-κB p65 levels in the PBMCs compared with those of healthy controls. However, patients with complicated P. falciparum malaria had decreased levels of phospho-NF-κB p65. On day 7 post-treatment, significantly increased phospho-NF-κB p65 was found in the PBMCs of patients with complicated P. falciparum, compared with healthy controls. The plasma level of IL-10 was elevated in day 0 in patients with complicated P. falciparum malaria and was found to be negatively correlated with phospho-NF-κB p65 level (rs = -0.630, p = 0.038). However, there was no correlation between phospho-NF-κB p65 expression and TNF level in patients with complicated P. falciparum malaria. CONCLUSIONS: This is the first report demonstrating alterations in NF-κB p65 activity in the PBMCs of malaria patients. The altered lower features of NF-κB p65 in the PBMCs of patients with complicated P. falciparum at admission could be due to a suppressive effect of high IL-10 associated with complicated P. falciparum malaria.|
|Appears in Collections:||TM-Article|
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