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Berghei Sporozoites (berghei + sporozoite)

Distribution by Scientific Domains
Medical Sciences57%
Life Sciences42%

Kinds of Berghei Sporozoites

  • plasmodium berghei sporozoite
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    Selected Abstracts

    Cross-protection between attenuated Plasmodium berghei and P. yoelii sporozoites

    PARASITE IMMUNOLOGY, Issue 11 2007
    M. SEDEGAH
    SUMMARY An attenuated Plasmodium falciparum sporozoite (PfSPZ) vaccine is under development, in part, based on studies in mice with P. berghei. We used P. berghei and P. yoelii to study vaccine-induced protection against challenge with a species of parasite different from the immunizing parasite in BALB/c mice. One-hundred percent of mice were protected against homologous challenge. Seventy-nine percent immunized with attenuated P. berghei sporozoite (PbSPZ) (six experiments) were protected against challenge with P. yoelii sporozoite (PySPZ), and 63% immunized with attenuated PySPZ (three experiments) were protected against challenge with PbSPZ. Antibodies in sera of immunized mice only recognized homologous sporozoites and could not have mediated protection against heterologous challenge. Immunization with attenuated PySPZ or PbSPZ induced CD8+ T cell-dependent protection against heterologous challenge. Immunization with attenuated PySPZ induced CD8+ T cell-dependent protection against homologous challenge. However, homologous protection induced by attenuated PbSPZ was not dependent on CD8+ or CD4+ T cells, and depletion of both populations only reduced protection by 36%. Immunization of C57BL/10 mice with PbSPZ induced CD8+ T cell-dependent protection against P. berghei, but no protection against P. yoelii. The cross-protection data in BALB/c mice support testing a human vaccine based on attenuated PfSPZ for its efficacy against P. vivax. [source]

    The immune status of Kupffer cells profoundly influences their responses to infectious Plasmodium berghei sporozoites

    EUROPEAN JOURNAL OF IMMUNOLOGY, Issue 8 2005
    Nick Steers
    Abstract Multi-factorial immune mechanisms underlie protection induced with radiation-attenuated Plasmodia sporozoites (,-spz). Spz pass through Kupffer cells (KC) before invading hepatocytes but the involvement of KC in protection is poorly understood. In this study we investigated whether ,-spz-immune KC respond to infectious spz in a manner that is distinct from the response of naive KC to infectious spz. KC were isolated from (1) naive, (2) spz-infected, (3) ,-spz-immune, and (4) ,-spz-immune-challenged C57BL/6 mice and examined for the expression of MHC class I and II, CD40 and CD80/CD86, IL-10 and IL-12 responses and antigen-presenting cell (APC) function. KC from ,-spz-immune-challenged mice up-regulated class I and costimulatory molecules and produced elevated IL-12p40, relative to naive KC. In contrast, KC from naive mice exposed to infectious spz down-modulated class I and IL-12p40 was undetectable. Accordingly, KC from spz-infected mice had reduced APC function, while KC from ,-spz-immune-challenged mice exhibited augmented APC activity. The nearly opposite responses are consistent with the fact that spz challenge of ,-spz-immune mice results in long-lasting sterile protection, while infection of naive mice always results in malaria. [source]

    The liver stage of Plasmodium berghei inhibits host cell apoptosis

    MOLECULAR MICROBIOLOGY, Issue 3 2005
    Claudia Van De Sand
    Summary Plasmodium berghei is the causative agent of rodent malaria and is widely used as a model system to study the liver stage of Plasmodium parasites. The entry of P. berghei sporozoites into hepatocytes has extensively been studied, but little is known about parasite,host interaction during later developmental stages of the intracellular parasite. Growth of the parasite far beyond the normal size of the host cell is an important stress factor for the infected cell. Cell stress is known to trigger programmed cell death (apoptosis) and we examined several apoptotic markers in P. berghei -infected cells and compared their level of expression and their distribution to that of non-infected cells. As none of the apoptotic markers investigated were found altered in infected cells, we hypothesized that parasite infection might confer resistance to apoptosis of the host cell. Treatment with peroxide or serum deprivation induced apoptosis in non-infected HepG2 cells, whereas P. berghei -infected cells appeared protected, indicating that the parasite interferes indeed with the apoptotic machinery of the host cell. To prove the physiological relevance of these results, mice were infected with high numbers of P. berghei sporozoites and treated with tumour necrosis factor (TNF)-,/d -galactosamine to induce massive liver apoptosis. Liver sections of these mice, stained for degraded DNA, confirmed that infected cells containing viable parasites were protected from programmed cell death. However, in non-treated control mice as well as in TNF-,-treated mice a small proportion of dead intracellular parasites with degraded DNA were detected. Most hepatocytes containing dead parasites provoked an infiltration of immunocompetent cells, indicating that these cells are no longer protected from cell death. [source]

    An early commitment to expression of a particular TCRV, chain on CD8+ T cells responding to attenuated Plasmodium berghei sporozoites is maintained following challenge with infectious sporozoites

    PARASITE IMMUNOLOGY, Issue 9-10 2010
    J. M. LUMSDEN
    Summary Protection induced by irradiated Plasmodium berghei sporozoites (Pb,-spz) in mice is linked to CD8+ T cells specific for exo-erythrocytic-stage Ags, and intrahepatic memory CD8+ T cells are associated with protracted protection. However, the Ag specificity of the protective CD8+ T cells remains largely unknown. In this study, we characterized the TCR V, usage by intrahepatic CD8+ T cells during ,-spz immunization and after the challenge with infectious Pb sporozoites. The repertoire of naïve (TN) and central memory (TCM) CD8+ T cells was diverse and conserved between individual mice, and did not change with immunization. In contrast, preferential usage of one or more TCR V, subset was observed in effector memory (TEM) CD8+ T cells after immunization. The expanded TCR V, varied between individual mice but V,4, 6, 7, 8.3, 9 and 11 were the most frequently expressed. In addition, there was a correlation in the TCR V, usage by ,-spz-induced CD8+ TEM in the liver and blood of individual mice. The expansion pattern of blood CD8+ TEM did not change with challenge and remained the same for 8 weeks thereafter. These results demonstrate that immunization with ,-spz skews the TCR V, repertoire of CD8+ TEM, and commitment to a particular TCR V, expression is maintained long-term. [source]

    Motility and infectivity of Plasmodium berghei sporozoites expressing avian Plasmodium gallinaceum circumsporozoite protein

    CELLULAR MICROBIOLOGY, Issue 5 2005
    Rita Tewari
    Summary Avian and rodent malaria sporozoites selectively invade different vertebrate cell types, namely macrophages and hepatocytes, and develop in distantly related vector species. To investigate the role of the circumsporozoite (CS) protein in determining parasite survival in different vector species and vertebrate host cell types, we replaced the endogenous CS protein gene of the rodent malaria parasite Plasmodium berghei with that of the avian parasite P. gallinaceum and control rodent parasite P. yoelii. In anopheline mosquitoes, P. berghei parasites carrying P. gallinaceum and rodent parasite P. yoelii CS protein gene developed into oocysts and sporozoites. Plasmodium gallinaceum CS expressing transgenic sporozoites, although motile, failed to invade mosquito salivary glands and to infect mice, which suggests that motility alone is not sufficient for invasion. Notably, a percentage of infected Anopheles stephensi mosquitoes showed melanotic encapsulation of late stage oocysts. This was not observed in control infections or in A. gambiae infections. These findings shed new light on the role of the CS protein in the interaction of the parasite with both the mosquito vector and the rodent host. [source]

    Fluorescent Plasmodium berghei sporozoites and pre-erythrocytic stages: a new tool to study mosquito and mammalian host interactions with malaria parasites

    CELLULAR MICROBIOLOGY, Issue 6 2001
    Ramya Natarajan
    To track malaria parasites for biological studies within the mosquito and mammalian hosts, we constructed a stably transformed clonal line of Plasmodium berghei, PbFluspo, in which sporogonic and pre-erythrocytic liver-stage parasites are autonomously fluorescent. A cassette containing the structural gene for the FACS-adapted green fluorescent protein mutant 2 (GFPmut2), expressed from the 5, and 3, flanking sequences of the circumsporozoite (CS) protein gene, was integrated and expressed at the endogenous CS locus. Recombinant parasites, which bear a wild-type copy of CS, generated highly fluorescent oocysts and sporozoites that invaded mosquito salivary glands and were transmitted normally to rodent hosts. The parasites infected cultured hepatocytes in vitro, where they developed into fluorescent pre-erythrocytic forms. Mammalian cells infected by these parasites can be separated from non-infected cells by fluorescence activated cell sorter (FACS) analysis. These fluorescent insect and mammalian stages of P. berghei should be useful for phenotypic studies in their respective hosts, as well as for identification of new genes expressed in these parasite stages. [source]