Host responses induced in mice by a radiation-attenuated Plasmodium berghei (NK65) malaria parasite

Suzuki, Mamoru; Waki, Seiji; Igarashi, Ikuo; Tamura, Jun’ichi; Imanaka, Motoo; Ishikawa, Shinsuke

doi:10.1016/0047-0740(80)90032-7

Cited by 6 publications

(2 citation statements)

References 7 publications

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“…Plasmoduim berghei XAT ( Pb XAT) is an irradiation-induced attenuated variant obtained from the lethal Pb NK65 strain. Blood-stage Pb XAT parasites were used in all experiments ( 20 ).…”

Section: Methodsmentioning

confidence: 99%

Plasmodium berghei infection ameliorates atopic dermatitis‐like skin lesions in NC/Nga mice

Kishi

Amano

Suzue

et al. 2014

Allergy

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BackgroundAtopic diseases are more prevalent in industrialized countries than in developing countries. In addition, significant differences in the prevalence of allergic diseases are observed between rural and urban areas within the same country. This difference in prevalence has been attributed to what is called the ‘hygiene hypothesis’. Although parasitic infections are known to protect against allergic reactions, the mechanism is still unknown. The aim of this study was to investigate whether or not malarial infections can inhibit atopic dermatitis (AD)-like skin lesions in a mouse model of AD.MethodsWe used NC/Nga mice which are a model for AD. The NC/Nga mice were intraperitoneally infected with 1 × 105 Plasmoduim berghei (Pb) XAT-infected erythrocytes.ResultsMalarial infections ameliorated AD-like skin lesions in the NC/Nga mice. This improvement was blocked by the administration of anti-asialo GM1 antibodies, which are anti-natural killer (NK) cells. Additionally, adoptive transfer of NK cells markedly improved AD-like skin lesions in conventional NC/Nga mice; these suggest that the novel protective mechanism associated with malaria parasitic infections is at least, in part, dependent on NK cells.ConclusionsWe have experimentally demonstrated for the first time that malarial infections ameliorated AD-like skin lesions in a mouse model of AD. Our study could explain in part the mechanism of the ‘hygiene hypothesis’, which states that parasitic infections can inhibit the development of allergic diseases.

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“…Plasmoduim berghei XAT ( Pb XAT) is an irradiation-induced attenuated variant obtained from the lethal Pb NK65 strain. Blood-stage Pb XAT parasites were used in all experiments ( 20 ).…”

Section: Methodsmentioning

confidence: 99%

Plasmodium berghei infection ameliorates atopic dermatitis‐like skin lesions in NC/Nga mice

Kishi

Amano

Suzue

et al. 2014

Allergy

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“…We have described an irradiation-induced attenuated variant of the normally lethal Plasmodium berghei that causes a self-limiting infection in Balb/c mice (Suzuki, Waki, Igarishi, Tamura, Imanaka & Ishikawa, 1980;Waki, Tamura, Imanaka, Ishikawa & Suzuki, 1982). This variant, P. berghei XAT, causes a greater degree of spleen enlargement than its virulent parent (Suzuki et al 1980) and, unlike its parent, it mainly parasitizes immature red cells (Waki et al 1982). Another interesting difference, which may be associated with virulence, is that the lethal parent induces the production of antilymphocyte autoantibodies whereas P. berghei XAT does not (Waki, Targett, de Souza & Playfair, 1984).…”

Section: Introductionmentioning

confidence: 99%

Immunity to an attenuated variant ofPlasmodium berghei: role of some non-specific factors

Waki

Taverne

et al. 1985

Parasitology

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Plasmodium berghei XAT, an attenuated variant of lethal P. berghei, causes a resolving infection in Balb/c mice from which they recover in about 3 weeks. The parasitaemia displays an early peak at about 5 days, followed by a steep drop in parasite number associated with the appearance of degenerating forms inside mature erythrocytes; the parasites remaining are inside reticulocytes. By contrast, no degenerating parasites were seen in infections caused by the virulent parent, which was mainly confined to mature erythrocytes. However, P. berghei XAT was no more sensitive to reactive O2 metabolites, generated by alloxan, or to tumour necrosis serum, than its virulent parent. Furthermore, its early drop in parasitaemia was unaffected by silica. The drop still occurred in the absence of T cells, although the infection was then ultimately lethal, and it was not mediated by NK cells since it occurred in nude mice treated with anti-asialo GM1 serum to abolish NK cell activity. However, it was absent in splenectomized mice, in which P. berghei XAT infection was lethal. Thus, the attenuation of P. berghei XAT infection is not due to increased susceptibility to some of the agents thought to cause parasite destruction, but to some other mechanism in which the spleen is involved.

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A marker epitope of attenuated Plasmodium berghei

et al. 1988

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Plasmodium berghei XAT is an irradiation-induced, permanent attenuated derivative from high-virulence P. berghei NK65. Monoclonal antibodies against XAT were developed. By immunofluorescence screening, one monoclonal antibody was identified that was reactive with XAT at the schizont stage but not with NK65 nor with any other stage of intra-erythrocytic development of either parasite. The monoclonal antibody precipitated a 240-kD molecule from metabolically labeled XAT antigens. This molecule was thought to be a marker epitope of the attenuated parasite.

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Host responses induced in mice by a radiation-attenuated Plasmodium berghei (NK65) malaria parasite

Cited by 6 publications

References 7 publications

Plasmodium berghei infection ameliorates atopic dermatitis‐like skin lesions in NC/Nga mice

Plasmodium berghei infection ameliorates atopic dermatitis‐like skin lesions in NC/Nga mice

Immunity to an attenuated variant ofPlasmodium berghei: role of some non-specific factors

A marker epitope of attenuated Plasmodium berghei

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