Macrophages as effector cells in immunity to malaria

Playfair, John; Dockrell, Hazel M.; Taverne, Janice

doi:10.1016/0165-2478(85)90173-7

Cited by 21 publications

(10 citation statements)

References 33 publications

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“…The mechanism by which malaria parasites induce inflammatory mediators is central to an understanding of anti-parasitic immunity and the factors that determine clinical outcome. It is widely supposed that the early phase of the inflammatory response is similar to that induced by bacteria, whereby microbial products such as LPS directly stimulate monocytes and macrophages to release TNF and other cytokines [3,27,28]. Our results suggest that this view is incomplete and that the early inflammatory response to malaria is critically dependent on macrophage-lymphocyte interactions.…”

Section: Discussionmentioning

confidence: 68%

Early cytokine induction by Plasmodium falciparum is not a classical endotoxin-like process

Scragg¹,

Hensmann²,

Bate³

et al. 1999

Eur. J. Immunol.

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We have investigated the widely held view that malaria parasites induce pro-inflammatory cytokines primarily through an endotoxin-like stimulatory effect on macrophages. We report that the pattern of cytokine production by non-immune human peripheral blood mononuclear cells following stimulation by Plasmodium falciparum-infected erythrocytes (Pfe) in vitro differs considerably from that induced by bacterial endotoxin. The Pfe-induced TNF response at day 1 is associated with a much higher level of IFN-gamma production and a much lower level of IL-12 p40 and IL-10 expression than a comparable endotoxin-induced TNF response. Both CD3(+) and CD14(+) populations are required for this early TNF response to Pfe, whereas the endotoxin-induced response is unaffected by depletion of the CD3(+) population. Pfe fails to stimulate the monocyte-like cell line MonoMac6 to express pro-inflammatory cytokines. These findings suggest that the early inflammatory response to malaria is critically dependent on lymphocyte subpopulations that play a lesser role in the response to bacterial endotoxin.

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Section: Discussionmentioning

confidence: 68%

Early cytokine induction by Plasmodium falciparum is not a classical endotoxin-like process

Scragg¹,

Hensmann²,

Bate³

et al. 1999

Eur. J. Immunol.

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“…p.i., postinoculation. involving mononuclear phagocytes is believed to play a role (42,53). There is a considerable body of evidence consistent with the concept that phagocyte-derived ROS are involved in host immunity against malaria infection (36).…”

Section: Fig 3 (A) Primary P Berghei Anka Infection In Gpx1mentioning

confidence: 96%

“…More than half a billion people are infected with malaria each year, and many of these infections result in chronic parasitemia and anemia. It is believed that phagocytic cells such as monocytes are important in the clearance of the blood-stage parasite (42,53). However, the mechanism by which monocytes and other phagocytic cells effect killing of the parasite is as yet unknown.…”

mentioning

confidence: 99%

Phagocyte-Derived Reactive Oxygen Species Do Not Influence the Progression of Murine Blood-Stage Malaria Infections

et al. 2005

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Phagocyte-derived reactive oxygen species have been implicated in the clearance of malaria infections. We investigated the progression of five different strains of murine malaria in gp91 phox؊/؊ mice, which lack a functional NADPH oxidase and thus the ability to produce phagocyte-derived reactive oxygen species. We found that the absence of functional NADPH oxidase in the gene knockout mice had no effect on the parasitemia or total parasite burden in mice infected with either resolving (Plasmodium yoelii and Plasmodium chabaudi K562) or fatal (Plasmodium berghei ANKA, Plasmodium berghei K173 and Plasmodium vinckei vinckei) strains of malaria. This lack of effect was apparent in both primary and secondary infections with P. yoelii and P. chabaudi. There was also no difference in the presentation of clinical or pathological signs between the gp91 phox؊/؊ or wild-type strains of mice infected with malaria. Progression of P. berghei ANKA and P. berghei K173 infections was unchanged in glutathione peroxidase-1 gene knockout mice compared to their wild-type counterparts. The rates of parasitemia progression in gp91 phox؊/؊ mice and wild-type mice were not significantly different when they were treated with L-N G -methylarginine, an inhibitor of nitric oxide synthase. These results suggest that phagocyte-derived reactive oxygen species are not crucial for the clearance of malaria parasites, at least in murine models.

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“…However, there was a slow steady expansion of macrophages in the spleen during the acute phase of the infection probably, reflecting the increased need for removal of infected erythrocytes in the spleen through phagocytosis or the production of proinflammatory cytokines (25,27).…”

Section: Discussionmentioning

confidence: 99%

Cellular Changes and Apoptosis in the Spleens and Peripheral Blood of Mice Infected with Blood-StagePlasmodium chabaudi chabaudiAS

2000

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Infection with blood-stage Plasmodium chabaudi chabaudi AS results in splenomegaly, peripheral leukocytosis, and a major activation of the immune system. The frequencies and absolute numbers of T-cell, B-cell, and macrophage populations in spleen and peripheral blood from P. chabaudi-infected BALB/c mice were compared and found to be significantly altered during acute infection. The kinetics of the redistribution of the different cell types in spleen and peripheral blood were different, with T and B cells appearing in the blood when their frequencies and absolute numbers in the spleen were low. The frequency and absolute number of apoptotic cells in the spleen were increased during acute P. chabaudi infection and involved both T cells, B cells, and macrophages. Both Fas and Fas-ligand expression were increased in the spleen. Taken together, our data provide new information on the complex cellular interactions that take place in the immune system during blood-stage malaria infection in a mouse model.

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Macrophages as effector cells in immunity to malaria

Cited by 21 publications

References 33 publications

Early cytokine induction by Plasmodium falciparum is not a classical endotoxin-like process

Early cytokine induction by Plasmodium falciparum is not a classical endotoxin-like process

Phagocyte-Derived Reactive Oxygen Species Do Not Influence the Progression of Murine Blood-Stage Malaria Infections

Cellular Changes and Apoptosis in the Spleens and Peripheral Blood of Mice Infected with Blood-StagePlasmodium chabaudi chabaudiAS

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