Experimental Parasitology

1982

DOI: 10.1016/0014-4894(82)90076-5

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Plasmodium berghei: Isolation and maintenance of an irradiation attenuated strain in the nude mouse

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Jun’ichi Tamura

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et al.

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Parasites and Infections1

Infection With Pb Xat But Not Pb 17x Induces Protective Immu1

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Cited by 52 publications

(35 citation statements)

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“…Pb NK65 is a high-virulence strain and was originally obtained from Dr. M. Yoeli (New York University Medical Center, New York, NY). Pb XAT is a low-virulence derivative from Pb NK65 (15). A nonlethal isolate of Py 17X was originally obtained from Dr. J. Finnerty (National Institutes of Health, Bethesda, MD) and cloned by limiting dilution.…”

Section: Parasites and Infectionsmentioning

confidence: 99%

“…It has been shown that mice infected with Pb NK65 develop severe parasitemia and die within 2 wk, although mice infected with Pb XAT or Py 17X cure spontaneously around 3 wk of infection (15,17). To examine whether primary infection with each of the two nonlethal parasites can induce protective immunity against Pb NK65 lethal infection, groups of C57BL/6 (B6) mice were infected with Pb XAT or Py 17X then challenged with Pb NK65 on day 30 after primary infection.…”

Section: Infection With Pb Xat But Not Pb 17x Induces Protective Immumentioning

confidence: 99%

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

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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.

“…Pb NK65 is a high-virulence strain and was originally obtained from Dr. M. Yoeli (New York University Medical Center, New York, NY). Pb XAT is a low-virulence derivative from Pb NK65 (15). A nonlethal isolate of Py 17X was originally obtained from Dr. J. Finnerty (National Institutes of Health, Bethesda, MD) and cloned by limiting dilution.…”

Section: Parasites and Infectionsmentioning

confidence: 99%

“…It has been shown that mice infected with Pb NK65 develop severe parasitemia and die within 2 wk, although mice infected with Pb XAT or Py 17X cure spontaneously around 3 wk of infection (15,17). To examine whether primary infection with each of the two nonlethal parasites can induce protective immunity against Pb NK65 lethal infection, groups of C57BL/6 (B6) mice were infected with Pb XAT or Py 17X then challenged with Pb NK65 on day 30 after primary infection.…”

Section: Infection With Pb Xat But Not Pb 17x Induces Protective Immumentioning

confidence: 99%

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

¹

,

²

,

³

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.

“…Therefore, we assessed the outcome of concomitant malaria/RF infection in mice by monitoring growth of the rodent malaria parasite P. berghei and the spirochete B. duttonii daily from day 3 postinfection. In mice, P. berghei infection is lethal (27), whereas infection with B. duttonii is generally not fatal (18). In experiments in which mice were infected only with P. berghei, 49.5% of the erythrocytes were parasitized (here referred to as parasitemia) at day 14 postinfection (Fig.…”

Section: Resultsmentioning

confidence: 99%

Concomitant Infection Decreases the Malaria Burden but Escalates Relapsing Fever Borreliosis

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et al. 2010

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About 500 million cases of malaria occur annually. However, a substantial number of patients who actually have relapsing fever (RF) Borrelia infection can be misdiagnosed with malaria due to similar manifestations and geographic distributions of the two diseases. More alarmingly, a high prevalence of concomitant infections with malaria and RF Borrelia has been reported. Therefore, we used a mouse model to study the effects of such mixed infection. We observed a 21-fold increase in spirochete titers, whereas the numbers of parasitized erythrocytes were reduced 15-fold. This may be explained by polarization of the host immune response toward the intracellular malaria parasite, resulting in unaffected extracellular spirochetes and hosts that succumb to sepsis. Mixed infection also resulted in severe malaria anemia with low hemoglobin levels, even though the parasite counts were low. Overall, coinfected animals had a higher fatality rate and shorter time to death than those with either malaria or RF single infection. Furthermore, secondary malaria infection reactivated a quiescent RF brain infection, which is the first evidence of a clinically and biologically relevant cue for reactivation of RF Borrelia infection. Our study highlights the importance of investigating concomitant infections in vivo to elucidate the immune responses that are involved in the clinical outcome.In the developing world, concomitant infections are the rule rather than the exception, and the complete clinical picture involves several microorganisms that influence each other as well as the host (8). Malaria is by far the most devastating acute febrile illness in humans, and it is caused by parasitic protozoa of the genus Plasmodium. The World Health Organization (WHO) has estimated that this disease is responsible for 1.5 to 2.7 million deaths annually, and about 1 million of those cases occur in children under the age of 5 years (24,28). Considering that the most prominent symptom of malaria is fever (4) and that the WHO advises that a presumptive malaria diagnosis be made in areas where malaria is endemic, it is plausible that misdiagnoses can be made in patients who are not suffering from malaria or who have a concomitant infection (14). This assumption is supported by the results of a field study conducted by our research team in Togo, West Africa, in which 8.8% of febrile patients diagnosed as having malaria were subsequently found to have relapsing fever (RF) borreliosis, which is caused by spirochete bacteria of the genus Borrelia (21). This could be simply due to incorrect malaria diagnosis, which is plausible since both Plasmodium and RF Borrelia cause systemic infections with similar manifestations that involve recurrent fever, anemia, and hepatosplenomegaly. It could also be due to malaria/RF coinfection, which makes a correct diagnosis even more complex. Moreover, medical personnel are generally not aware of the existence of RF borreliosis, even though the incidence of that condition in countries such as Senegal is the highest des...

“…Such approaches have been repeated in mice using otherwise lethal infections of P. berghei [14,15] and Plasmodium yoelii [16]. From these, a number of sporozoite surface antigens have already been identified and considered as vaccine candidates, but it is still in limited success.…”

Section: Introductionmentioning

confidence: 99%

Evaluation of Immune Response in Mouse Blood Post Injection with Gamma Ray-Attenuated Sporozoites of Plasmodium berghei

et al. 2014

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Abstract:Ionizing radiation has been successfully used to attenuate parasites for malaria vaccine development. To get a deeper insight in the immune response post injection of irradiated pre-erythrocytic stage of malaria parasites (sporozoites), we used Plasmodium berghei as a model. Anopheles sp. with infective parasites in their salivary glands was irradiated with 0-225 Gy of gamma rays. The isolated sporozoites were intravenously injected into groups of mouse followed by a booster and challenge in interval time of 2-4 weeks. The detection of parasite in the infected mosquito was done with nested-PCR (polymerase chain reaction). Immune response in mouse blood was examined with ELISA (enzime-linked immunosorbent assay) and protein profile of irradiated sporozoites was studied with SDS-PAGE (sodium dodecyl sulphate-polyacrylamide gel electrophoresis). By using Anopheles farauti as the more susceptible mosquito to parasite infection, based on molecular detection and parasites observation in mouse blood, there was low or no effect of irradiated sporozoites on the immune responses in mouse serum. Some factors affecting these results are discussed. There was a slight alteration of protein profile of sporozoite infected salivary glands post gamma ray irradiation except for its band intensity, indicating the low effectiveness of gamma irradiation at optimal dose. It can be concluded that irradiated sporozoite as vaccine materials was failed in eliciting immune response.

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