Plasmodium falciparum parasites induce interferon production in human peripheral blood ‘null’ cells in vitro

Rönnblom, Lars; Ojo-Amaize, Emmanuel A.; Wigzell, Hans; Alm, Gunnar V.

doi:10.1111/j.1365-3024.1983.tb00734.x

Cited by 12 publications

(6 citation statements)

References 20 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Therefore, they thought that NK cells might be protective in the early stages of malarial infection. Other workers have also reported the involvement of NK cells in P. falciparum infection in humans (Rönnblom et al 1983;Theander et al 1987;Orago and Facer 1991) and in P. berghei infection in rats (Solomon 1986). NK cells are thought to have nonspecific immunity and not to be involved in immunological memory.…”

Section: Discussionmentioning

confidence: 94%

“…Eugui and Allison (1980) reported that mouse strains resistant to P. chabaudi infection showed high natural killer (NK) activities, whereas other workers reported that there was no relationship between NK activity and protection against P. chabaudi infection using NK-celldeficient mice (Wood and Clark 1982;Skamene et al 1983). There are, however, some findings suggesting that NK cells play certain roles in protection against plasmodial infection: cytotoxicity of human NK cells to schizonts of P. falciparum (Orago and Facer 1991), natural cytotoxicity of rat spleen cells to P. berghei-parasitized erythrocytes (Solomon 1986), and the possible relevance of the interferon (IFN) and NK cell system in P. falciparum infection (Rönnblom et al 1983). In the present study we investigated whether NK cells were involved in the protection against P. chabaudi infection by transferring NK cells from immune mice to naive mice and by depleting the hosts' NK cells with an anti-NK1.1 monoclonal antibody (mAb).…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Analysis of roles of natural killer cells in defense against Plasmodium chabaudi in mice

Kitaguchi

Nagoya

Amano

et al. 1996

Parasitology Research

View full text Add to dashboard Cite

Mice that have recovered from a primary infection with Plasmodium chabaudi have been shown to resist a secondary infection. In the present study the authors investigated how natural killer (NK) cells were involved in this resistance. Spleen cells from P. chabaudiprimed C57BL/6 mice could transfer protection against P. chabaudi infection into naive syngeneic mice, but spleen cells from unprimed mice could not. T-enriched cells purified from primed spleen cells could also transfer such protection. Transfer of NK cells from primed spleen cells failed to protect against challenge infection. However, depletion of NK cells in host mice by injection of an anti-NK1.1 monoclonal antibody resulted in higher mortality relative to controls. The possible protective roles of NK cells in P. chabaudi infection are discussed.

show abstract

Section: Discussionmentioning

confidence: 94%

Section: Introductionmentioning

confidence: 99%

Analysis of roles of natural killer cells in defense against Plasmodium chabaudi in mice

Kitaguchi

Nagoya

Amano

et al. 1996

Parasitology Research

View full text Add to dashboard Cite

show abstract

“…In pilot experiments, the depletion of NK cells during the early phase of infection did not impact the day or the magnitude of peak parasitemia (not shown). However, it is increasingly accepted that NK cells can produce cytokines that augment proinflammatory responses during P. chabaudi and P. falciparum infection (4,33), and direct recognition of P. falciparuminfected erythrocytes by human NK cells has been described by use of in vitro systems (1,2,28,34,42). Further studies will be required to determine the impact of early stimulation of NK cells by malarial infection on the nature of the subsequent immune response.…”

Section: Discussionmentioning

confidence: 99%

Experimental Malaria Infection Triggers Early Expansion of Natural Killer Cells

et al. 2008

View full text Add to dashboard Cite

In order to gain a better understanding of gene expression during early malaria infection, we conducted microarray analysis of early blood responses in mice infected with erythrocytic-stage Plasmodium chabaudi. Immediately following infection, we observed coordinated and sequential waves of immune responses, with interferon-associated gene transcripts dominating by 16 h postinfection, followed by strong increases in natural killer (NK) cell-associated and major histocompatibility complex class I-related transcripts by 32 h postinfection. We showed by flow cytometry that the observed elevation in NK cell-associated transcripts was the result of a dramatic increase in the proportion of NK cells in the blood during infection. Subsequent microarray analysis of NK cells isolated from the peripheral blood of infected mice revealed a cell proliferation expression signature consistent with the observation that NK cells replicate in response to infection. Early proliferation of NK cells was directly observed in studies with adoptively transferred cells in infected mice. These data indicate that the early response to P. chabaudi infection of the blood is marked by a primary wave of interferon with a subsequent response by NK cells.

show abstract

“…There have been few reports to date that suggest that IFN-␣ is produced during falciparum malaria infection. [42][43][44][45] As mixed infections of P falciparum and P vivax are frequent in several malaria-endemic regions, 46 it is tempting to speculate that in coinfected humans, IFN-␣ induced by P falciparum infection could block the production of reticulocytes and inhibit the development of P vivax. This clearly deserves further study.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of Plasmodium yoelii blood-stage malaria by interferon α through the inhibition of the production of its target cell, the reticulocyte

Vigário

Belnoue

Cumano

et al. 2001

Blood

View full text Add to dashboard Cite

The effect of a recombinant hybrid human interferon ␣ (IFN-␣) (which cross-reacts with murine cells) on C57BL/6 mice infected with Plasmodium yoelii sporozoites or parasitized erythrocytes was determined. IFN-␣ did not inhibit the development of the parasite in the liver, but it did reduce the blood parasite load and the hepatosplenomegaly induced by the infection in mice injected with blood-stage parasites. The extent of anemia in IFN-␣-treated and control mice was similar, despite the lower parasite load in the IFN-␣-treated mice.The reduced blood parasite load in IFN-␣-treated mice was associated with reduced erythropoiesis and reticulocytosis. As reticulocytes are the preferred target cells for the strain of P yoelii used (P yoelii yoelii 265 BY), it was postulated that the inhibition of reticulocytosis in IFN-␣-treated mice was causally related to the observed decreased blood parasite load. This was supported by the finding that IFN-␣ inhibited a different strain of P yoelii (17X clone A), which also displays a tropism for reticulocytes, but not a line of Plasmodium vinckei petteri, which infects only mature red blood cells. As human malaria species also display different tropism for reticulocytes, these findings could be relevant for people co- IntroductionMalaria remains a disease that is estimated to kill 1.5 million to 2.7 million people each year. 1 The parasite and its mosquito vector have become resistant to several drugs in recent years, and this has stimulated a search for new therapeutic strategies. Recombinant cytokines can confer protection against bacterial, viral, and some intracellular parasitic infection. Some of these cytokines can also inhibit the development of the malaria parasite. Recombinant interferon ␥ (IFN-␥) inhibits the development of the liver stage of murine, 2 simian, 3 and human 3,4 malaria in vitro and in vivo. Protection against murine and simian malaria is also obtained after treatment with recombinant (r) IL-12. [5][6][7] Type I interferons were originally described as potent antivirus substances that are produced by animal cells infected with virus. However, the role of type I IFNs in the defense against nonvirus pathogen is much less well studied. 8 IFN type I (IFN-␣ or ␤) inducers, such as Newcastle disease virus, statolon, or polyriboinosinic-polyribocytidylic acid, 9-13 and unpurified serum IFN 14 protect against Plasmodium berghei infection. However, the action of IFN-␣ alone is still not known.In this study, we have analyzed the effect of a recombinant human IFN-␣ hybrid that cross-reacts with murine cells on the course and the pathology of infection with different species or strains of rodent Plasmodium, initiated by inoculation with either sporozoites or parasitized erythrocytes. We show that inhibition of parasite-induced reticulocytemia by IFN-␣ influences only parasite species that are restricted to reticulocytes. Our results extend previous observations 15 whose interpretation is complicated by the fact that a corticosteroid, which is a potent immunosuppresso...

show abstract

Plasmodium falciparum parasites induce interferon production in human peripheral blood ‘null’ cells in vitro

Cited by 12 publications

References 20 publications

Analysis of roles of natural killer cells in defense against Plasmodium chabaudi in mice

Analysis of roles of natural killer cells in defense against Plasmodium chabaudi in mice

Experimental Malaria Infection Triggers Early Expansion of Natural Killer Cells

Inhibition of Plasmodium yoelii blood-stage malaria by interferon α through the inhibition of the production of its target cell, the reticulocyte

Contact Info

Product

Resources

About