Inactivation of Plasmodium falciparum Parasites Using g-irradiation

Ferreira-da-Cruz, Maria de Fátima; Têva, Antônio; Espindola-Mendes, Erika da Cruz; Santos, Luciana Ferreira dos; Daniel-Ribeiro, Cláudio Tadeu

doi:10.1590/s0074-02761997000100029

Cited by 10 publications

(7 citation statements)

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“…Prior to injection, the blood cells were exposed to a dose of 200 Gy gamma-radiation from a Gamma Cell 200 Irradiator (Atomic Energy of Canada, Ltd., Ottawa, Canada) utilizing a 60 Co source located at the Research Center of the College of Science, King Saud University, Saudi Arabia. This radiation dose was applied based on experiments conducted by Ferreira-da-Cruz et al [ 30 ], which provided evidence that a 200-Gy gamma-irradiation dose abolishes the original replication of erythrocytic forms of the Palo Alto P . falciparum strain, most likely by inactivating their infectivity.…”

Section: Methodsmentioning

confidence: 99%

Infection of Female BWF1 Lupus Mice with Malaria Parasite Attenuates B Cell Autoreactivity by Modulating the CXCL12/CXCR4 Axis and Its Downstream Signals PI3K/AKT, NFκB and ERK

et al. 2015

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Systemic lupus erythematosus (SLE) is a prototypic autoimmune disease characterized by abnormal autoreactivity in B cells. Lymphocytes and their soluble mediators contribute to the disease pathogenesis. We recently demonstrated that infecting lupus mice with malaria confers protection against lupus nephritis by attenuating oxidative stress in both liver and kidney tissues. In the current study, we further investigated B cell autoreactivity in female BWF1 lupus mice after infection with either live or gamma-irradiated malaria, using ELISA, flow cytometry and Western blot analysis. The lupus mice exhibited a significant elevation in plasma levels of IL-4, IL-6, IL-7, IL-12, IL-17, IFN-α, IFN-γ, TGF-β, BAFF and APRIL and a marked elevation of IgG2a, IgG3 and ant-dsDNA autoantibodies compared with normal healthy mice. Infecting lupus mice with live but not gamma-irradiated malaria parasite partially and significantly restored the levels of the soluble mediators that contribute to the progression of lupus. Furthermore, the B cells of lupus mice exhibited an increased proliferative capacity; aberrant overexpression of the chemokine receptor CXCR4; and a marked elevation in responsiveness to their cognate ligand (CXCL12) via aberrant activation of the PI3K/AKT, NFκB and ERK signaling pathways. Interestingly, infecting lupus mice with live but not gamma-irradiated malaria parasite restored a normal proliferative capacity, surface expression of CXCR4 and B cell response to CXCL-12. Taken together, our data present interesting findings that clarify, for the first time, the molecular mechanisms of how infection of lupus mice with malaria parasite controls B cell autoreactivity and thus confers protection against lupus severity.

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Section: Methodsmentioning

confidence: 99%

Infection of Female BWF1 Lupus Mice with Malaria Parasite Attenuates B Cell Autoreactivity by Modulating the CXCL12/CXCR4 Axis and Its Downstream Signals PI3K/AKT, NFκB and ERK

et al. 2015

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“…Prior to injection, the blood cells were exposed to a dose of 200 Gy gamma-radiation from a Gamma Cell 200 Irradiator (Atomic Energy of Canada, Ltd., Ottawa, Canada) utilizing a 60 Co source located at the Research Center of College of Science, King Saud University, Saudi Arabia. This radiation dose was applied based on experiments conducted by Ferreira-da-Cruz et al [23] that provided evidence that a 200-Gy gamma-irradiation dose is able to abolish the original replication of erythrocytic forms of the Palo Alto P. falciparum strain, most likely by inactivating their infectivity. According to their data, 100 or 150 Gy irradiation doses were unable to inactivate the parasite, despite the reduction of parasitemia.…”

Section: Methodsmentioning

confidence: 99%

Malarial Infection of Female BWF1 Lupus Mice Alters the Redox State in Kidney and Liver Tissues and Confers Protection against Lupus Nephritis

Al‐Quraishy

Abdel-Maksoud

Elamir

et al. 2013

Oxidative Medicine and Cellular Longevity

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Systemic lupus erythematosus (SLE) is a prototypic autoimmune disease characterized by an imbalanced redox state and increased apoptosis. Tropical infections, particularly malaria, may confer protection against SLE. Oxidative stress is a hallmark of SLE. We have measured changes in the levels of nitric oxide (NO), hydrogen peroxide (H2O2), malondialdehyde (MDA), and reduced glutathione (GSH) in both kidney and liver tissues of female BWF1 lupus mice, an experimental model of SLE, after infection with either live or gamma-irradiated malaria. We observed a decrease in NO, H2O2, and MDA levels in kidney tissues after infection of lupus mice with live malaria. Similarly, the levels of NO and H2O2 were significantly decreased in the liver tissues of lupus mice after infection with live malaria. Conversely, GSH levels were obviously increased in both kidney and liver tissues after infection of lupus mice with either live or gamma-irradiated malaria. Liver and kidney functions were significantly altered after infection of lupus mice with live malaria. We further investigated the ultrastructural changes and detected the number of apoptotic cells in kidney and liver tissues in situ by electron microscopy and TUNEL assays. Our data reveal that infection of lupus mice with malaria confers protection against lupus nephritis.

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“…Experiments conducted by Ferreira-da-Cruz et al [37] in Brazil provide evidences that a 200 Gy gamma-irradiation is able to abolish the original replication of erythrocytic forms of the Palo Alto P. falciparum strain, probably by inactivating their infectivity. According to their data, 100 or 150 Gy irradiation doses were enable to inactivate the parasite, despite the reduction of parasitemia, suggesting the existence of heterogenous plasmodial populations as concerns susceptibility to irradiation and pointing to the possibility that the same dose could inactivate parasites from other P. falciparum strains.…”

Section: Dose Of Irradiation As Crucial Factormentioning

confidence: 98%