Activation of nuclear factor kappa B in peripheral blood mononuclear cells from malaria patients

Malaria Journal

Research

Noppadon Tangpukdee¹  Kwannan Nantavisai²  Rachanee Udomsangpetch³  Srivicha Krudsood⁴  Urai Chaisri⁵  Parnpen Viriyavejakul⁶  Yaowapa Maneerat⁶  Chuchard Punsawad⁶  Emsri Pongponratn⁶ 

[1] Department of Clinical Tropical Medicine, Faculty of Tropical Medicine, Mahidol University, 420/6 Rajvithi Road, 10400, Bangkok, Thailand;Center for Emerging and Neglected Infectious Diseases, Mahidol University, 10400, Bangkok, Thailand;Department of Microbiology, Faculty of Medicine, Srinakarinwiroj University, 114 Sukumvit 23, 10110, Bangkok, Thailand;Department of Pathobiology, Faculty of Science, Mahidol University, 272 Rama VI Road, Ratchathewi, 10400, Bangkok, Thailand;Center for Emerging and Neglected Infectious Diseases, Mahidol University, 10400, Bangkok, Thailand;Department of Tropical Hygiene, Faculty of Tropical Medicine, Mahidol University, 420/6 Rajvithi Road, 10400, Bangkok, Thailand;Center for Emerging and Neglected Infectious Diseases, Mahidol University, 10400, Bangkok, Thailand;Department of Tropical Pathology, Faculty of Tropical Medicine, Mahidol University, 420/6 Rajvithi Road, 10400, Bangkok, Thailand;Department of Tropical Pathology, Faculty of Tropical Medicine, Mahidol University, 420/6 Rajvithi Road, 10400, Bangkok, Thailand;Center for Emerging and Neglected Infectious Diseases, Mahidol University, 10400, Bangkok, Thailand;

关键词: Malaria;    Plasmodium falciparum;    Plasmodium vivax;    Nuclear factor kappa B;    Peripheral blood mononuclear cells;    Interleukin-10;    Tumor necrosis factor;   

DOI  :  10.1186/1475-2875-11-191

 received in 2012-03-12, accepted in 2012-06-10,  发布年份 2012

来源: Springer

【 摘 要 】

BackgroundMalaria 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.MethodsThe 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.ResultsAt 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.ConclusionsThis 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.

【 授权许可】

Unknown   
© Punsawad et al.; licensee BioMed Central Ltd. 2012. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.