Plasmodium berghei XAT: Contribution of γδ T cells to host defense against infection with blood-stage nonlethal malaria parasite

Kobayashi, Fuminori; Niikura, Mamoru; Waki, Seiji; Matsui, Toshihiro; Fujino, Takashi; Tsuruhara, Takashi; Kamiya, Shigeru

doi:10.1016/j.exppara.2007.05.002

Cited by 18 publications

(34 citation statements)

References 36 publications

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“…An ELISA for the detection of IFN-␥ or IL-10 in plasma was conducted as described previously (16). A rat anti-mouse IFN-␥ (clone R4 -6A2; eBioscience) and a rat anti-mouse IL-10 (clone JES5-16E3; eBioscience) were used as the capture Abs, and a biotin-coupled rat anti-mouse IFN-␥ (clone XMG1.2; eBioscience) and IL-10 (clone JES5-2A5; eBioscience) were used as the detecting Abs.…”

Section: Cytokine Assaymentioning

confidence: 99%

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Coinfection with Nonlethal Murine Malaria Parasites Suppresses Pathogenesis Caused by Plasmodium berghei NK65

Niikura

Kamiya

Kita

et al. 2008

The Journal of Immunology

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Mixed infection with different Plasmodium species is often observed in endemic areas, and the infection with benign malaria parasites such as Plasmodium vivax or P. malariae has been considered to reduce the risk of developing severe pathogenesis caused by P. falciparum. However, it is still unknown how disease severity is reduced in hosts during coinfection. In the present study, we investigated the influence of coinfection with nonlethal parasites, P. berghei XAT (Pb XAT) or P. yoelii 17X (Py 17X), on the outcome of P. berghei NK65 (Pb NK65) lethal infection, which caused high levels of parasitemia and severe pathogenesis in mice. We found that the simultaneous infection with nonlethal Pb XAT or Py 17X suppressed high levels of parasitemia, liver injury, and body weight loss caused by Pb NK65 infection, induced high levels of reticulocytemia, and subsequently prolonged survival of mice. In coinfected mice, the immune response, including the expansion of B220intCD11c+ cells and CD4+ T cells and expression of IL-10 mRNA, was comparable to that in nonlethal infection. Moreover, the suppression of liver injury and body weight loss by coinfection was reduced in IL-10−/− mice, suggesting that IL-10 plays a role for a reduction of severity by coinfection with nonlethal malaria parasites.

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Section: Cytokine Assaymentioning

confidence: 99%

“…Flow cytometric analysis was performed on single-cell suspensions of spleen and peripheral blood cells as described previously (16). Total spleen cell numbers in uninfected and infected mice are shown in Table I.…”

Section: Flow Cytometrymentioning

confidence: 99%

Coinfection with Nonlethal Murine Malaria Parasites Suppresses Pathogenesis Caused by Plasmodium berghei NK65

Niikura

Kamiya

Kita

et al. 2008

The Journal of Immunology

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“…The nitric oxide (NO) concentration in plasma was measured using the QuantiChrom nitric oxide assay kit (BioAssay Systems). The malarial antigens were prepared from the erythrocytic stages as described previously (26,27). Malaria-specific antibodies in the plasma of mice were assayed using soluble antigens from P. berghei XAT as the capture antigens.…”

Section: Animals and Parasitesmentioning

confidence: 99%

Development of Severe Pathology in Immunized Pregnant Mice Challenged with Lethal Malaria Parasites

et al. 2013

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b Pregnant women are highly susceptible to malaria infection because of their low immunity and are at increased risk of maternal illness or death, in addition to spontaneous abortion, stillbirth, premature delivery, and low birth weight. However, the detailed pathogenesis of maternal malaria remains unclear. In this study, we evaluated a mouse model that shows similar severe pathological features of pregnant women during Plasmodium falciparum infection and investigated the pathogenesis of maternal malaria. Pregnant mice immunized by infection with an attenuated parasite, Plasmodium berghei XAT, were more susceptible to virulent P. berghei NK65 challenge/infection than were nonpregnant mice and showed high levels of parasitemia and a poor pregnancy outcome associated with placental pathology, such as accumulation of parasitized red blood cells, in the late phase of pregnancy. Notably, the pregnant immune mice challenged/infected with P. berghei NK65 developed liver injury associated with microvesicular fatty infiltration in late pregnancy. The pathological features were similar to acute fatty liver of pregnancy. Higher levels of gamma interferon and nitric oxide (NO) were found in plasma from pregnant immune mice infected with P. berghei NK65 than in plasma from nonpregnant mice. These findings suggest that development of liver injury and placental pathology in pregnant immune mice challenged/infected with P. berghei NK65 is accompanied by enhanced production of proinflammatory cytokines. Malaria is the most devastating parasitic disease of humans in tropical and subtropical regions, resulting in an estimated 0.6 to 1 million deaths per year (1). The populations at greatest risk of developing severe pathology are children under the age of 5 years and pregnant women in areas where Plasmodium falciparum is endemic (2-4). Every year, approximately 50 million women living in areas where malaria is endemic become pregnant. An estimated 10,000 of these women and 200,000 of their fetuses or infants die annually as a result of malaria during pregnancy (1, 2). Malaria during pregnancy is a major public health problem in areas of endemicity, especially in Africa.People living in regions where malaria is endemic acquire protective immunity against malaria parasites and often show asymptomatic infection. However, women are highly susceptible to malaria infection because of their low immunity during pregnancy and are at increased risk of maternal illness or death (5, 6). Malaria during pregnancy, in addition to maternal illness or death, is implicated in the occurrence of spontaneous abortion, stillbirth, premature delivery, and low birth weight (6). Recently, it has been demonstrated that pregnant mice infected with lethal Plasmodium berghei parasites show a feature similar to placental pathology and subsequently poor pregnancy outcome (7,8).Cerebral malaria (CM) or respiratory distress syndrome has been reported to be an infrequent but relevant cause of maternal death in women living in an area of sub-Saharan Africa where m...

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“…We previously reported that mice depleted of γδ T cells using mAb could not eliminate the nonlethal malaria parasite strain Plasmodium berghei XAT (9), which is an attenuated variant of the lethal strain P. berghei NK65 (10). Therefore, γδ T cells are important for protective immunity against blood-stage malaria (9). However, the precise cellular and molecular mechanisms of the γδ T-cell-involved protective immunity against malaria parasites remain unknown.…”

mentioning

confidence: 99%

“…Therefore, γδ T cells may have protective or pathological effects on blood-stage malaria. We previously reported that mice depleted of γδ T cells using mAb could not eliminate the nonlethal malaria parasite strain Plasmodium berghei XAT (9), which is an attenuated variant of the lethal strain P. berghei NK65 (10). Therefore, γδ T cells are important for protective immunity against blood-stage malaria (9).…”

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confidence: 99%

Enhancement of dendritic cell activation via CD40 ligand-expressing γδ T cells is responsible for protective immunity toPlasmodiumparasites

Inoue

Niikura

Takeo

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

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Previous reports have shown that γδ T cells are important for the elimination of malaria parasites in humans and mice. However, how γδ T cells are involved in protective immunity against blood-stage malaria remains unknown. We infected γδ T-cell–deficient (TCRδ-KO) mice and control wild-type mice with Plasmodium berghei XAT, which is a nonlethal strain. Although infected red blood cells were eliminated within 30 d after infection, TCRδ-KO mice could not clear the infected red blood cells, showed high parasitemia, and eventually died. Therefore, γδ T cells are essential for clearance of the parasites. Here, we found that γδ T cells play a key role in dendritic cell activation after Plasmodium infection. On day 5 postinfection, γδ T cells produced IFN-γ and expressed CD40 ligand during dendritic cell activation. These results suggest that γδ T cells enhance dendritic cell activation via IFN-γ and CD40 ligand–CD40 signaling. This hypothesis is supported strongly by the fact that in vivo induction of CD40 signaling prevented the death of TCRδ-KO mice after infection with P . berghei XAT. This study improves our understanding of protective immunity against malaria and provides insights into γδ T-cell–mediated protective immunity against various infectious diseases.

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Plasmodium berghei XAT: Contribution of γδ T cells to host defense against infection with blood-stage nonlethal malaria parasite

Cited by 18 publications

References 36 publications

Coinfection with Nonlethal Murine Malaria Parasites Suppresses Pathogenesis Caused by Plasmodium berghei NK65

Coinfection with Nonlethal Murine Malaria Parasites Suppresses Pathogenesis Caused by Plasmodium berghei NK65

Development of Severe Pathology in Immunized Pregnant Mice Challenged with Lethal Malaria Parasites

Enhancement of dendritic cell activation via CD40 ligand-expressing γδ T cells is responsible for protective immunity toPlasmodiumparasites

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