ACCELERATED CLEARANCE OF UNINFECTED RED CELLS FROM <i>PLASMODIUM BERGHEI</i>‐INFECTED MOUSE BLOOD IN NORMAL MICE

Howard, Russell J.; Mitchell, Graham F.

doi:10.1038/icb.1979.46

Cited by 14 publications

(9 citation statements)

References 4 publications

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“…By this procedure, it is possible to collect approximately 1.5 X 10* uninfected cells/h from blood of 50% parasitemia, together with approximately 5 X 10ŝ ingly infected cells, 3 X 10^ cells with two nuclei and 3X10" cells with ^ three nuclei. This collection rate has been sufficient for studies with ^'Cr-labeled or cell surface radiolabeled samples (Howard & Mitchell 1979, Howard et al 1980a. A proportion of the parasite-infected cells obtained by this procedure are still viable in terms of inducing lethal infections of naive hosts (Howard & Battye 1979).…”

Section: B Cell Separation Proceduresmentioning

confidence: 99%

“…However, these studies did not use 100% pure uninfected RBCs from an infected animal of high parasitemia. We therefore devised a method for labeling RBCs from P. berghei-infected mice with both *'Cr and the DNA-binding dye 33258 Hoechst (Howard & Mitchell 1979), and used the FACS method described above (Section II, B.) to isolate pure "Cr-labeled uninfected cells (i.e., nonfiuorescent cells).…”

Section: G Clearance Of Uninfected Rbcs From Infected Bloodmentioning

confidence: 99%

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Alterations in the Surface Membrane of Red Blood Cells During Malaria

Howard

1982

Immunological Reviews

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Section: B Cell Separation Proceduresmentioning

confidence: 99%

Section: G Clearance Of Uninfected Rbcs From Infected Bloodmentioning

confidence: 99%

Alterations in the Surface Membrane of Red Blood Cells During Malaria

Howard

1982

Immunological Reviews

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“…falciparurn malaria by Facer et a1 (1979). In an animal malaria, P. bergkei, the clearance of NPRBC in non-parasitized mice was more rapid than the clearance of normal red cells (Howard & Mitchell, 1979).…”

mentioning

confidence: 94%

“…Extensive phagocytosis of PKBC seen in the bone marrow during life and the spleen at post mortem has been observed (Spitz, 1946: Clark & Tomlinson, 1949Abdalla et ul, 1980). In an animal malaria, P. bergkei, the clearance of NPRBC in non-parasitized mice was more rapid than the clearance of normal red cells (Howard & Mitchell, 1979). Phagocytosis of NPRBC by monocytes was also observed in four children with I-'.…”

mentioning

confidence: 94%

Reduced erythrocyte survival following clearance of malarial parasitaemia in Thai patients

Looareesuwan

Merry²,

Phillips

et al. 1987

Br J Haematol

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Erythrocyte survival times were measured in healthy Thai controls and in patients following clearance of asexual P. falciparum or P. vivax parasitaemia. In five controls the mean cell life (MCL) of compatible donor erythrocytes was 89.6 d (mean range 73-101 d) compared with a mean MCL of 56.8 d (range 30-66 d) for autologous erythrocytes in 12 falciparum patients. In one of these patients the survival curve was biphasic with a rapid loss of some labelled cells. The survival of compatible donor erythrocytes was also studied in 10 patients and two types of survival curve could be distinguished. In five patients the cells had a mean MCL of 64.4 d (range 42-90 d). In the others survival curves were curvilinear, suggesting a complex mechanism of cell clearance or the presence of more than one cell population. There was initially a more rapid rate of destruction. In P. vivax malaria the MCL of autologous erythrocytes in seven patients was a mean of 67.2 d (range 34-74 d) and that of compatible donor cells in six patients was 66.8 d (range 54-76 d). In all except one of these patients both autologous and donor cell survival curves could be fitted to straight lines. No increase in cell-bound IgG or C3 was evident in 12 patients tested. The differences between the mean MCL in all the groups of patients and the controls were statistically significant at the 5% level. This indicates an increased rate of erythrocyte destruction following clearance of P. falciparum or P. vivax parasites which is not antibody or complement mediated. The mechanism is unknown, but appears to be extrinsic to the erythrocytes themselves and may result from nonspecific activation of the reticuloendothelial function associated with the parasitic infection.

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“…Several factors could lead to anemia, including the hemolysis of infected erythrocytes, spleen removal of noninfected red blood cells, or the destruction of infected and noninfected erythrocytes by the immune system [37,38]. An additional possible factor causing anemia could be reduced erythrocyte recycling resulting from the production of proinflammatory cytokines or noneffective maturation of erythrocytes [37].…”

Section: Discussionmentioning

confidence: 98%

Altered Nucleotide Receptor Expression in a Murine Model of Cerebral Malaria

Marín-García¹,

Sánchez-Nogueiro²,

Díez³

et al. 2009

J INFECT DIS

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In cerebral malaria, the most severe complication of malaria, both neurotransmission mechanisms and energy metabolism are affected. To understand how metabolic changes modify neurotransmission, we examined P2 receptor expression in a murine model of cerebral malaria. Quantitative polymerase chain reaction experiments revealed that parasite deposition was greatest in the cerebellum, compared with other areas of the brain, suggesting a correlation between brain parasitemia and loss of control of movement. Infected mice showed modified patterns of expression of P2 receptor subtype messenger RNA (mRNA), depending on both the specific purinergic receptor and the cerebral region analyzed. Immunohistochemical studies indicated altered levels of protein expression by these receptors in infected brains and, in some cases, a pattern of expression different from that noted in control mice. These differences in both the amount of mRNA and the protein distribution of P2 receptors observed in the different brain sites in infected mice suggest an important role for P2 receptors in either provoking cerebral damage or conferring neuroprotection.

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ACCELERATED CLEARANCE OF UNINFECTED RED CELLS FROM PLASMODIUM BERGHEI‐INFECTED MOUSE BLOOD IN NORMAL MICE

Abstract: Summary 51Cr‐labelled uninfected cells, separated from Plasmodium berghei‐infected mouse blood using the fluorescence‐activated cell sorter, were cleared more rapidly than normal mouse erythrocytes after intravenous injection into normal mice.

Cited by 14 publications

References 4 publications

Alterations in the Surface Membrane of Red Blood Cells During Malaria

Alterations in the Surface Membrane of Red Blood Cells During Malaria

Reduced erythrocyte survival following clearance of malarial parasitaemia in Thai patients

Altered Nucleotide Receptor Expression in a Murine Model of Cerebral Malaria

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