Shahid Waseem; Kashif-Ur-Rehman -; Ramesh Kumar; Tariq Mahmood
Volume 13, Issue 1 , March 2016, , Pages 1-8
Abstract
Background: Falciparum malaria is a severe health burden worldwide. Antigen presenting cells are reported to be affected by erythrocytic stage of the parasite. Malarial hemozoin (HZ), a metabolite of malaria parasite, has adjuvant properties and may play a role in the induction of immune response against ...
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Background: Falciparum malaria is a severe health burden worldwide. Antigen presenting cells are reported to be affected by erythrocytic stage of the parasite. Malarial hemozoin (HZ), a metabolite of malaria parasite, has adjuvant properties and may play a role in the induction of immune response against the parasite. Objective: To determine the immunological impact of hemozoin on the capacity of innate immune cells maturation. Methods: Plasmodium falciparum (F32 strain) was cultured in O+ blood group up to 18% parasitemia. Natural hemozoin was extracted from infected red blood cells. Murine bone marrow derived macrophages and myeloid dendritic cells were stimulated with 4 ߤg/mL or 40 ߤg/mL of synthetic hemozoin (β-hematin) or natural hemozoin. We assessed the immunomodulatory role of synthetic or natural hemozoin in vitro by flowcytometric analysis. Results: The maturation markers MHCII, CD80 and CD86 were significantly upregulated (p<0.05) on the surface of murine bone marrow derived macrophages or myeloid dendritic cells. Data confirmed the potential of macrophages or myeloid dendritic cells, through hemozoin activation, to establish an innate immune response against malaria parasites. Conclusion: Both synthetic and natural hemozoin are potent inducers of cellular immunity against malaria infection. However, natural hemozoin is a stronger inducer as compared to synthetic hemozoin.
Ganiyu Arinola; Chris Ezeh
Volume 4, Issue 1 , March 2007, , Pages 44-49
Abstract
Background: Sickle cell disease (HbSS) is a major health problem in Nigeria and ma-laria has been implicated as a leading cause of morbidity/mortality in sickle cell disease patients. Few reasons were put forward to explain the observed morbidity/mortality of HbSS subjects due to Plasmodium falciparum ...
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Background: Sickle cell disease (HbSS) is a major health problem in Nigeria and ma-laria has been implicated as a leading cause of morbidity/mortality in sickle cell disease patients. Few reasons were put forward to explain the observed morbidity/mortality of HbSS subjects due to Plasmodium falciparum (P. falciparum) malaria. Objectives: To determine the level of immunoglobulin classes (IgM, IgA, and IgG) and regulators of complement system (C1 inhibitor and C3 activator) in Nigerian HbSS patients with and without P. falciparum parasitemia. Methods: A total of 64 subjects were considered, including 10 HbSS genotypic subjects with P. falciparum parasitemia (HbSS+PfM), 18 HbAA genotypic subjects with P. falciparum parasitemia (HbAA+PfM), 20 HbSS without P. falciparum parasitemia (HbSS-PfM), and 16 HbAA genotypic subjects with-out P. falciparum parasitemia (HbAA-PfM). IgM, IgA, IgG, C1 inhibitor, and C3 acti-vator titers were quantified by single radial immunodiffusion method. Results: The mean levels of IgG in HbSS+PfM (2373.90±1772.81mg/dl) and HbAA+PfM (1868.80±0.00mg/dl) were significantly higher compared with HbSS-PfM (644.55±171.15mg/dl) or HbAA-PfM (659.75±158.01mg/dl) patients. HbAA-PfM sub-jects had the lowest level of IgM (67.27±63.7mg/dl), though no significant difference was observed comparing mean levels of IgM between the four groups. IgA titer was significantly higher in HbSS-PfM patients (249.00±94.8mg/dl) compared with HbAA-PfM (p<0.05), HbAA+PfM (p<0.05), or HbSS+PfM (p<0.05). The mean values of C1 inhibitor were lower in HbSS+PfM and HbAA+PfM compared with HbSS-PfM or HbAA-PfM. However, HbAA+PfM had a significantly lower value of C1 inhibitor compared with HbAA-PfM (p<0.01). C3 activator was highest in HbSS-PfM (17.10±7.35mg/dl) and was significantly higher compared with HbSS+PfM (p<0.05). Conclusion: Increased C1 inhibitor and decreased C3 activator in HbSS+PfM com-pared with HbAA+PfM shows that deranged regulation of complement factors may be responsible for increased susceptibility of HbSS to P. falciparum malaria.
