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At least 19 recordsLinked to original sources
PubMed1989

Molecular karyotyping of the rodent malarias Plasmodium chabaudi, Plasmodium berghei and Plasmodium vinckei.

The molecular karyotypes of four isolates of Plasmodium chabaudi, three of the subspecies P. chabaudi adami and one P. chabaudi chabaudi, as well as P. berghei and P. vinckei were studied by means of pulsed field gradient (PFG) gel electrophoresis. Each species appears to have 14 chromosomes, ranging in size from approximately 730 kb to greater than 2000 kb. The three P. chabaudi adami isolates did not appear any more similar to each other than to the P. c. chabaudi isolate. The chromosome locations of genes for a heat shock protein (hsp) 70, ribosomal RNA (rRNA), the precursor to the major merozoite surface proteins, dihydrofolate reductase and P. falciparum antigen 352 as well as four cloned DNA markers and a telomere probe were determined. However, a number of probes representing cloned P. falciparum antigens failed to hybridize to P. chabaudi DNA. Hence genes for malaria antigens appear to be much more divergent than genes for housekeeping functions.

Animals↗
PubMedDate not supplied

Aminopeptidases from Plasmodium falciparum, Plasmodium chabaudi chabaudi and Plasmodium berghei.

Using fluorogenic substrates and polyacrylamide gels we detected in cell-free extracts of Plasmodium falciparum, Plasmodium chabaudi chabaudi and Plasmodium berghei only a single aminopeptidase. A comparative study of the aminopeptidase activity in each extract revealed that the enzymes have similar specificities and kinetics, a near-neutral pH optima of 7.2 and are moderately thermophilic. Each has an apparent molecular weight of 80,000 +/- 10,000, determined by high performance liquid chromatography on a calibrated SW500 column. Whilst the P. c. chabaudi and P. berghei activity co-migrate in native polyacrylamide gels, that of P. falciparum migrates more slowly. The three enzymes can be selectively inhibited by ortho-phenanthroline and are thus metallo-aminopeptidases; however, in contrast to other aminopeptidases the metal co-factor does not appear to be Zn2+.

Aminopeptidases↗
PubMed1987

The effect of mosquito transmission of antigenic variants of Plasmodium chabaudi.

Plasmodium chabaudi AS strain in mice is characterized by an acute primary parasitaemia, and one or more less acute recrudescences. Previous work has shown, using a passive protection assay, that the recrudescent parasites are usually antigenically different from parasites of the parent population with which the mice were first infected. In this study the effect of mosquito transmission on the antigenic expression of recrudescent populations of P. chabaudi was examined. In the first experiments the recrudescent population which was antigenically different from the parent population was uncloned. After transmission through Anopheles stephensi the recrudescent population appeared to revert to an antigenic type similar to that of the parent population. In the second experiment clones from a recrudescent population were mosquito transmitted and again the parasites of the primary patent parasitaemia in the mice, bitten by the infected mosquitoes, had reverted to the parental type. It is suggested that antigenic variants of P. chabaudi AS strain may revert to a basic type after mosquito transmission.

Animals↗
PubMed1985

Iron deficiency protects inbred mice against infection with Plasmodium chabaudi.

Plasmodium chabaudi infections of NFR/N mice made anemic by dietary iron deficiency produced mortalities of 25% (male) and 7% (female) compared with 100% in iron-sufficient controls. When iron-deficient mice convalescing from the primary infection were returned to the normal diet, 100% experienced recrudescent parasitemia. No recrudescence occurred in mice maintained on the iron-deficient diet.

Anemia, Hypochromic↗
PubMed1982

Adipose tissue lipoprotein lipase activity in Plasmodium chabaudi and Plasmodium vinckei rodent malaria.

Adipose tissue lipoprotein lipase activity (LPL) falls dramatically during experimental infection of mice by Plasmodium chabaudi. The decrease in this activity accounts for the seric accumulation of triacyl-glyceride-rich lipoproteins (chylomicrons mainly and Very Low Density Lipoproteins (VLDL) partly). This loss of tissue LPL enzyme activity is moreover enhanced, in capillary vessels, by a simultaneous decrease in the activatory power of serum towards the enzyme. This phenomenon is mainly related to the presence of Very Low Density Lipoproteins. In the mouse VLDL apoprotein composition is supposed to be modified. On the contrary, in fatal infection of mice by P. vinckei the adipose tissue lipoprotein lipase (LPL) activity is normal or even increased.

Adipose Tissue↗
PubMed1983

Serological cross-reaction between high molecular weight proteins synthesized in blood schizonts of Plasmodium yoelii, Plasmodium chabaudi and Plasmodium falciparum.

A 230 000 molecular weight (MW) Plasmodium yoelii protein, a 250 000 MW P. chabaudi protein and a 195 000 MW P. falciparum protein, identified using monoclonal antibodies, have similar characteristics, and have been implicated as protective antigens. In this study the serological relationship between these proteins was investigated by Western transfer analysis. The monoclonal antibodies specific for each of the high molecular weight proteins did not cross-react with antigens of the other two parasites, but a polyvalent mouse serum raised against the purified 230 000 MW P. yoelii protein cross-reacted with the high molecular weight proteins of P. chabaudi and P. falciparum and also with the fragments derived from these proteins. This result indicates that these proteins belong to the same class of malaria parasite antigen.

Amino Acid Sequence↗
PubMed1985

Gametocytogenesis and ribosomal rRNA gene organisation in the rodent malarias Plasmodium chabaudi and Plasmodium berghei.

A cloned Plasmodium berghei (ANKA) isolate was syringe passaged repeatedly to generate a line that was non-infective to Anopheles stephensi. Ribosomal gene organisation of this non-infective line was then compared to its infective ancestor. DNA was also prepared from asexual parasites and gametocytes of P. chabaudi and the arrangement of the rRNA genes of this species was studied. Although macrogametocytes have many more ribosomes than microgametocytes, this increase does not appear to stem from an amplification of the rRNA genes, as no differences either in the quantity or the arrangement of the rDNA could be detected. Furthermore, the loss of infectivity of the P. berghei gametocytes does not seem to be due to a reduction or rearrangement of sequences coding for the rRNA genes. P. chabaudi and P. berghei DNA failed to show any homology to a repetitive DNA sequence cloned from P. falciparum. We conclude that this probe, PFH8rep20, is specific for P. falciparum.

Animals↗
PubMed1985

Distribution of immunoglobulin isotypes in the nonspecific B-cell response induced by infection with Plasmodium chabaudi adami and Plasmodium yoelii.

The nonspecific B-cell response induced by infecting mice with two nonlethal malaria parasites, Plasmodium chabaudi adami and Plasmodium yoelii, was analyzed in an isotype-specific reverse plaque assay. Our results showed different isotypic patterns in the two infections, although cells secreting immunoglobulin of all isotypes were increased to some extent. P. yoelii induced large increases in secreting cells of all isotypes; IgG2a-secreting cells were increased out of proportion to those of the other IgG classes. P. chabaudi induced large increases in secreting cells of all isotypes except IgG1. In addition, there was not a disproportionate increase in cells secreting IgG2a. The data show that these "polyclonal" responses are different during each infection. There are marked similarities between the distribution of "nonspecific isotypes" and the specific antibodies formed in each infection.

Animals↗
PubMed1984

Immunoglobulin isotype distribution of malaria-specific antibodies produced during infection with Plasmodium chabaudi adami and Plasmodium yoelii.

The antibody response of mice to Plasmodium chabaudi adami and Plasmodium yoelii has been compared using a solid phase isotype-specific radioimmunoassay and sodium dodecyl sulfate-polyacrylamide gel electrophoresis. Serological cross-reactivity between these parasites was substantial. Studies using a radioimmunoassay detecting all classes of malaria-specific antibody demonstrated that during the early part of infection it was not possible to distinguish between homologous and heterologous reactions. Immunoprecipitation and sodium dodecyl sulfate-polyacrylamide gel electrophoresis revealed that 50% or more of the protein antigens detected were apparently shared by both parasites although the intensity of bands was always greater with homologous reactions. However, the distribution of isotypes in the antibody (Ab) response differed in the two infections. P. chabaudi infections were characterized by a predominant and persistent IgM response, moderate IgG2 and IgG3 and little significant IgG1 response during a primary infection. By contrast, IgM antibodies were transient in P. yoelii infection, IgG2 was the predominant isotype, and both IgG1 and IgG3 antibodies were present during a primary infection. These differences in isotypes were also detected when sera were tested on the heterologous antigen extracts suggesting that antigens shared by P. chabaudi and P. yoelii do not necessarily induce similar antibody responses in the two infections.

Animals↗
PubMed1988

Plasmodium chabaudi antigen Pch105, Plasmodium falciparum antigen Pf155, and erythrocyte band 3 share cross-reactive epitopes.

By immunoblotting with a number of monoclonal antibodies raised in human and murine malaria systems, we have been able to establish the presence of cross-reactive epitopes on the Plasmodium falciparum vaccine candidate antigen Pf155/RESA and its proposed Plasmodium chabaudi analog Pch105. These findings were confirmed when the same antibodies were tested in an immunofluorescence assay. By using short synthetic peptides corresponding to repeated sequences in the C terminus of the Pf155 and enzyme-linked immunosorbent assays, the cross-reacting epitope was found to be localized to this repeat segment. Furthermore, a monoclonal antibody to murine erythrocyte band 3 which also cross-reacted with human band 3 bound to both Pch105 and Pf155 as well as to the synthetic peptides, suggesting that these proteins share a related epitope. The cross-reactions reflect the existence of sequence homologies of band 3 with these plasmodial proteins. This molecular similarity may be used by the parasite to disturb the rigidity of the erythrocyte membrane, thereby facilitating its entrance into the cell.

Animals↗
PubMed2005

An AFLP-based genetic linkage map of Plasmodium chabaudi chabaudi.

BACKGROUND: Plasmodium chabaudi chabaudi can be considered as a rodent model of human malaria parasites in the genetic analysis of important characters such as drug resistance and immunity. Despite the availability of some genome sequence data, an extensive genetic linkage map is needed for mapping the genes involved in certain traits. METHODS: The inheritance of 672 Amplified Fragment Length Polymorphism (AFLP) markers from two parental clones (AS and AJ) of P. c. chabaudi was determined in 28 independent recombinant progeny clones. These, AFLP markers and 42 previously mapped Restriction Fragment Length Polymorphism (RFLP) markers (used as chromosomal anchors) were organized into linkage groups using Map Manager software. RESULTS: 614 AFLP markers formed linkage groups assigned to 10 of 14 chromosomes, and 12 other linkage groups not assigned to known chromosomes. The genetic length of the genome was estimated to be about 1676 centiMorgans (cM). The mean map unit size was estimated to be 13.7 kb/cM. This was slightly less then previous estimates for the human malaria parasite, Plasmodium falciparum CONCLUSION: The P. c. chabaudi genetic linkage map presented here is the most extensive and highly resolved so far available for this species. It can be used in conjunction with the genome databases of P. c chabaudi, P. falciparum and Plasmodium yoelii to identify genes underlying important phenotypes such as drug resistance and strain-specific immunity.

Alleles↗
PubMedDate not supplied

Immunisation with recombinant AMA-1 protects mice against infection with Plasmodium chabaudi.

The Plasmodium merozoite surface antigen apical membrane antigen-1 (AMA-1) has previously been shown to provide partial protection to Saimiri and rhesus monkeys immunised with recombinant Plasmodium fragile or parasite-derived Plasmodium knowlesi AMA-1, respectively. In the study reported here we have used the Plasmodium chabaudi/mouse model system to extend our pre-clinical assessment of an AMA-1 vaccine. We describe here the expression of the full-length Plasmodium chabaudi adami AMA-1 and the P. chabaudi adami AMA-1 ectodomain using both baculovirus and Escherichia coli. The ectodomain expressed in E. coli, which contained an N-terminal hexa-his tag, was purified by Ni-chelate chromatography and refolded in vitro in the presence of oxidised and reduced glutathione to generate intramolecular disulphide bonds. In a series of vaccine trials, in both inbred and outbred mice, highly significant protection was obtained by immunising with the refolded AMA-1 ectodomain. Protection was shown to correlate with antibody response and was dependent on intact disulphide bonds. Passive transfer of antibodies raised in rabbits against the refolded AMA-1 ectodomain was also protective. In view of this demonstration that E. coli expression of a soluble P. chabaudi AMA-1 domain can generate a vaccine that is effective in mice, we are pursuing a similar approach to generating a vaccine against P. falciparum for testing in human volunteers.

Animals↗