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D Camus

Publications and source records attributed to D Camus.

At least 91 records · Page 5Linked to original sources
PubMed1990

Primary structure of the 175K Plasmodium falciparum erythrocyte binding antigen and identification of a peptide which elicits antibodies that inhibit malaria merozoite invasion.

The Plasmodium falciparum gene encoding erythrocyte binding antigen-175 (EBA-175), a putative receptor for red cell invasion (Camus, D., and T. J. Hadley. 1985. Science (Wash. DC). 230:553-556.), has been isolated and characterized. DNA sequencing demonstrated a single open reading frame encoding a translation product of 1,435 amino acid residues. Peptides corresponding to regions on the deduced amino acid sequence predicted to be B cell epitopes were assessed for immunogenicity. Immunization of mice and rabbits with EBA-peptide 4, a synthetic peptide encompassing amino acid residues 1,062-1,103, produced antibodies that recognized P. falciparum merozoites in an indirect fluorescent antibody assay. When compared to sera from rabbits immunized with the same adjuvant and carrier protein, sera from rabbits immunized with EBA-peptide 4 inhibited merozoite invasion of erythrocytes in vitro by 80% at a 1:5 dilution. Furthermore, these sera inhibited the binding of purified, authentic EBA-175 to erythrocytes, suggesting that their activity in inhibiting merozoite invasion of erythrocytes is mediated by blocking the binding of EBA-175 to erythrocytes. Since the nucleotide sequence of EBA-peptide 4 is conserved among seven strains of P. falciparum from throughout the world (Sim, B. K. L. 1990. Mol. Biochem. Parasitol. 41:293-296.), these data identify a region of the protein that should be a focus of vaccine development efforts.

Amino Acid Sequence↗
PubMed1990

Immunoreactivity of neoglycolipids constructed from oligomannosidic residues of the Candida albicans cell wall.

To establish a model to study the immunoreactivity of oligosaccharidic structures from the Candida albicans cell wall, we attempted to construct neoglycolipids with these residues by using oligomannosides released after mild acid hydrolysis of the phosphopeptidomannans isolated from yeast forms. From a mixture of manno-oligosaccharides ranging from mannobiose to mannononaose, the structure of a quantitatively major component (mannotriose) was determined to be Man (beta 1-2) Man (beta 1-2) Man alpha by 1H nuclear magnetic resonance analysis. After coupling of the pool of oligosaccharides to a lipid (4-hexadecylaniline), the synthesized molecules were injected into mice and rats. Antibody responses were detected on enzyme-linked immunosorbent assay plates coated with either phosphopeptidomannans or neoglycolipids. The hybrid molecules exhibited both immunogenicity and antigenicity. The kinetics of antibody responses as well as immunofluorescence patterns observed on whole C. albicans cells strongly mimicked results from the immunization of animals with natural antigens. Construction of neoglycolipids could therefore provide an interesting approach to the study of specific oligosaccharides of C. albicans and their recognition by the host immune system.

Animals↗
PubMed1988

Protein p126: a parasitophorous vacuole antigen associated with the release of Plasmodium falciparum merozoites.

The p126 protein is synthesized by P. falciparum between the 32nd and the 36th hour of the erythrocytic cycle, and is localized in the parasitophorous vacuole. It is processed when schizonts rupture and the major fragments (50, 47 and 18 kDa), which are released into culture supernatant, have been characterized using monoclonal antibodies. The 47 kDa fragment has been mapped at the N-terminus of the molecule. The portion of the protein p126 gene coding for this fragment contains 3 introns and is characterized by a sequence coding for 6 repeats of 8 aminoacids and by repeats of TCA/T-AGT coding for a polyserine sequence of 37 serines in a row for the FCR-3 strain. The 50 kDa fragment is also found in culture supernatant when merozoites are released from mature schizonts. The incubation of mature schizonts with leupeptin inhibits the release of merozoites and, in this case, a 56 kDa intermediate product is found. In those conditions, merozoites were observed free in the erythrocyte cytoplasm, the membrane of the parasitophorous vacuole being destroyed. The 50 kDa fragment can be obtained from the 56 kDa fragment by treatment with trypsin (a protease inhibited by leupeptin). Our results suggest that the processing of the 56 kDa fragment: 1) is protease-dependent, and could depend on a trypsin-like activity; 2) cannot occur after the release of merozoites because of the protease inhibitors contained in the serum; 3) does not occur before the release of merozoites, since no processed products of the protein p126 are observed in unruptured schizonts.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acid Sequence↗
PubMed1988

[The rabbit, experimental host of Pneumocystis carinii].

Pneumocystis carinii can be collected from experimentally immunodepressed rats. However, development of experimental pneumocystosis in this host requires corticoid-treatment during 8 to 12 weeks while P. carinii can be obtained from immunodepressed rabbits after 2 to 4 weeks. In 400 to 650 g body weight-white rabbits normally fed, two immunodepression protocols were used: (a) daily subcutaneous injections of hydrocortisone acetate (10 mg/kg body weight) and G penicillin (25,000 IU)-streptomycin (3 mg); (b) continuous oral administration of prednisolone (20 mg/l/day) and amoxicillin (25 mg/l/day) both diluted in drinking water. Between 55 and 78% of rabbits treated by any immunodepression protocol died within 5-20 days after a terminal important diarrhoea. Seventy and seventy-seven per cent of the young rabbits respectively treated by protocols (a) or (b), showed the presence of Pneumocystis by the direct microscopic examination, but all of them were found positive after lung concentration. Fifty-five per cent of the older rabbits (950-1,400 g) were positive by pulmonary smear examination when treated with protocol (a). Pneumocystis obtained were good antigens for indirect immunofluorescence and immunoblot assays using human and rabbit sera.

Animals↗
PubMed1988

[Histopathology of the liver and kidney during malaria: relation to malaria-induced dyslipoproteinemia].

A kinetic study concerning histologic and cytologic alterations during Plasmodium chabaudi infection of Swiss mice has been carried out. In liver, a reversible focal and non ischemic necrosis and a vascular congestion were observed together with an accumulation of malarial pigment. The endoplasmic reticulum cisternae and Golgi saccules of hepatocytes were highly distended. Hepatocyte microvilli in biliary canaliculi and in Disse' spaces were markedly less developed and less numerous than in normal liver. Intracytoplasmic lipid globules were found in large amount in hepatocytes before the peak of parasitaemia. Their number and size gradually diminished thereafter. Hepatocytic mitochondria showed important unspecific modifications probably in relation, at last partly, to the tissue anoxia. Some hepatocytic changes (intracytoplasmic lipid globules, enlargement of endoplasmic reticulum cisternae and Golgi saccules) were consistent with an increased synthesis of lipoproteins (VLDL). The kidney showed only minor histological and ultrastructural changes. However haemosiderin was observed in proximal tubules and in their bordering cells. The deposit of immune complex reported previously do not appear associated with tissular or cellular important alterations.

Animals↗
PubMed1987

Characterization of gp195 processed products purified from Plasmodium falciparum culture supernates.

Schizonts of the malaria parasite Plasmodium falciparum synthesize a 195 kDa surface glycoprotein (gp195) that is processed into several smaller products including one of 83 kDa, which, in the case of the Camp strain, is sequentially processed into 73 and 67 kDa products. gp195 and its processing intermediates larger than 83 kDa were not precipitated from culture supernates, but the 83 and 73 kDa products were precipitated by three monoclonal antibodies (McAbs). The 83 and 73 kDa products were affinity purified from culture supernates by adsorbing to McAb 7B2 coupled to Affigel 10 and eluting either with 0.2 N acetic acid, pH 2.8, or with 3 M potassium isothiocyanate (KSCN). The epitope recognized by McAb 7B2 was denatured by acid elution but could be regenerated by treating with 8 M urea followed by dialysis. The implications of renaturing antigens to regenerate epitopes should be considered in studies on the purification, function and immunogenicity of malaria antigens.

Animals↗
PubMed1985

A Plasmodium falciparum antigen that binds to host erythrocytes and merozoites.

Antigens that bind to erythrocytes were identified in the supernatant fluids of a cultured human malaria parasite (Plasmodium falciparum). A 175-kilodalton (175K) antigen bound only to erythrocytes susceptible to invasion. The 175K antigen from the Camp or the FCR-3 strain also bound to merozoites. However, the antigen did not bind to merozoites when merozoites and supernatant antigens were from different strains unless proteinase inhibitors were present. Moreover, erythrocytes coated with supernatant antigens from the Camp or FCR-3 strain were invaded normally by merozoites of the homologous strain but were partially resistant to invasion by merozoites of the heterologous strain. The 175K antigen may be a receptor acting as a "bridge" between erythrocytes and merozoites.

Animals↗
PubMed1985

[Lipoproteins and malaria. I. Immunogenicity of serum lipoproteins in mice infected with Plasmodium chabaudi].

Anti-lipoprotein antibodies (anti-Lp Ab) have been investigated during the course of acute infection with P. chabaudi in Swiss mice using a radio-immunoprecipitation assay with (125)-iodine radiolabelled lipoproteins from normal or infected mice. Antibodies were detected 11 days after the beginning of infection; however, the highest lipoprotein precipitations were observed with purified (125)-I labelled lipoproteins from day-5 or day-7 infected mice. P. chabaudi infected mice were treated with chloroquine at various intervals after the beginning of infection and anti-Lp Ab were assayed on day 13. Anti-Lp Ab were not observed in mice treated before day 7 but were present in all mice treated after day 7. Anti-Lp Ab were not detected in mice infected with P. yoelii 17 X. Injection of purified lipoproteins from day-7 P. chabaudi infected mice (Lp day-7) to normal uninfected mice did not induce an antibody response to lipoproteins but anti-Lp Ab were observed when the same injection was performed in P. yoelii infected mice. Moreover, anti-Lp Ab were detected in uninfected mice injected concomitantly with Lp day-7 and hematin extracted from malarial pigment. Our results suggest that anti-Lp Ab observed in P. chabaudi infected mice are mainly against modified lipoproteins produced during infection and that the induction of the antibody response against lipoproteins requires an adjuvant effect such as the hematin which is released during infection.

Animals↗
PubMed1985

[Lipoproteins and malaria. II. Immunoregulatory role of immunoglobulin-lipoprotein complexes in mice infected with Plasmodium chabaudi on antibody producing cells].

Injection of lipoproteins from Plasmodium chabaudi infected mice into mice previously immunized with either human serum transferrin, bovine serum albumin, polyvinyl-pyrrolidone or tetanus toxoid, was followed by a decrease in the levels of antibodies directed against these antigens, suggesting a blockade of antibody secreting cells (Goumard et al., 1982). However, lipoproteins in P. chabaudi infected mice are complexed with immunoglobulins during the second week of infection (Demonchy et al., 1982). In this study, the effects of lipoproteins and Ig-lipoprotein complexes (Ig-Lp) on antibody secreting cells was investigated in vitro. Spleen cells from mice immunized with tetanus toxoid were cultured in microplates and the antitetanus antibodies (anti-TT Ab) were measured in the culture supernatants using a radioimmunoassay (Goumard et al., 1984). Ig-Lp purified from day-11 or day-13 P. chabaudi infected mice inhibited the secretion of anti-TT Ab when introduced into microcultures. On the contrary, lipoproteins purified from either day-5, day-7, day-21 or day-28 infected mice as well as lipoproteins from uninfected mice did not inhibit anti-TT Ab secreting cells. Ig-Lp formed in vitro with lipoproteins purified from day-7 infected mice (Lp J-7) and day-20 infected mice sera, inhibited anti-TT Ab secreting cells. IgG purified from day-20 sera and incubated with Lp J-7, inhibited anti-TT Ab secreting cells but no inhibitory effect was observed with the F(ab')2 fragments of these Ig. Pre-incubation of anti-TT Ab secreting cells with Fc fragments of mouse IgG blocked the inhibitory effect of Ig-Lp purified from infected mouse sera or formed in vitro.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

Renal deposits of lipoprotein-immunoglobulin complexes in Plasmodium chabaudi-infected mice.

Lipoprotein metabolism is altered and immunoglobulin-lipoprotein complexes (Ig-Lp) are formed during malaria infection (1-5). Ig-Lp were detected in the sera of Plasmodium chabaudi-infected mice 9 days post-infection (1 or 2 days after parasitemia had peaked at about 50%) and reached a maximum on day 13 (when the parasitemia had decreased to less than 1%). Renal glomerular deposits of IgM were first detected at day 3 and were heavy from day 9 to day 29; deposits of IgG and low density lipoprotein (LDL) were present from days 9 to 62, and were more dense from days 22 to 29; deposits of C3 were observed from day 13 to day 29. Apoprotein B component was found in heparin eluates of kidneys on day 10, 14, and 29. Fractionated Ig-Lp, as well as whole sera from day-13 infected mice, were injected into uninfected mice that developed LDL glomerular deposits only when pre-treated with histamine. LDL glomerular deposits were also observed after i.v. injection of day-29 sera (containing free anti-lipoprotein antibody) into day-7 infected mice, but not when a mixture of day-29 and day-7 sera was injected into normal recipient mice. LDL glomerular deposits, however, were observed when recipient mice were treated with the Plasmodium-derived Insoluble Material (PDIM) 3 days before the injection of the day-29-day-7 sera mixture or day-13 serum. Two hours after the i.v. injection of 125I-Ig-Lp, the radioactivity of the kidneys was higher in histamine-treated, PDIM-treated, and P. chabaudi-infected mice than in controls. The clearance of 125I-Ig-Lp was higher in infected and in PDIM-treated mice than in controls. We suggest that the glomerular deposit of Ig-Lp that occurs during P. chabaudi infection requires an enhancing factor such as PDIM that is released during infection.

Animals↗
PubMed1982

[Immunoglobulin-lipoprotein complexes during P. chabaudi infection].

Immunoglobulin-lipoprotein complexes have been investigated in the course of P. chabaudi acute infection of Swiss mice. Serum ultracentrifugation in a sucrose density gradient was used to demonstrate the presence of immunoglobulins in the enriched lipoprotein fraction of density lower than 1100. The levels of lipoprotein-bound immunoglobulins (Ig-Lp) were measured using the rate-nephelometric Immuno-Chemistry-System. IgM-Lp and IgG-Lp were significantly increased at day 9 and reached a peak at day 13 post-infection. From day 13 to day 16 they dramatically decreased. This kinetic effect was similar to that of non-specific circulating immune complexes detected by the [125I]Clq binding assay. A radioimmuno-precipitation-PEG-assay (RIPEGAssay) with [125I]Lp revealed the highest Lp precipitation with day 13 post-infection mouse sera compared to controls. Similar results were recorded when control sera were 8 times as concentrated in order to obtain Ig levels identical in both control and experimental sera. Part of the lipoprotein-bound immunoglobulins were demonstrated to be anti-Lp antibodies by the way of the RIPEGAssay using F(ab')2 fragments from infected mouse sera. Moreover, the [125I]Clq bound to the Ig-Lp complexes isolated from day 13 mouse sera. The present data suggest that the alteration of lipid metabolism which characterizes malaria infection could lead to the complexation of lipoproteins to immunoglobulins.

Animals↗
PubMed1981

Immunoregulation by Schistosoma mansoni.

Schistosoma mansoni is known to release an inhibitory factor of lymphocyte proliferation elicited in vitro. The effect of this dialyzable schistosome incubation product (DSIP) was tested in vivo on different aspects of the cell-mediated immune response. First, the DSIP injected into C57B1/6 mice markedly inhibited the delayed type hypersensitivity to sheep red blood cells (SRBC). Furthermore, the DSIP injected into S. mansoni infected Fisher rats at the beginning of the infection induced an inhibition of the specific lymphocyte response to S. mansoni antigen and of the spleen cell response to concanavalin A (Con A). The DSIP injected into uninfected rats also inhibited the spleen cell response to Con A. In uninfected as in infected rats injected with the DSIP, the lymphocyte response to Con A was restored after purification of the spleen cells on a nylon wool column. Moreover spleen cells from rats injected wtih the DSIP reduced the proliferative response of normal syngeneic spleen cells induced by Con A. This inhibition was not observed when cells from DSIP-injected rats were previously passed through a nylon wool column. In contrast, nylon wool depletion of spleen cells from infected rats injected with the DSIP did not restore the lymphocyte response to S. mansoni antigen. It seems tht DSIP could partly explain the modulation of the cellular immune responses observed during S. mansoni infection and could represent one of the mechanisms of this parasite's survival in the immunized host.

Animals↗
PubMed1981

Schistosoma mansoni: autoantibodies and polyclonal B cell activation in infected mice.

The appearance of autoantibodies was investigated during the course of Schistosoma mansoni infection in C57Bl/6 mice. Anti-liver autoantibodies or lymphocyte-reactive alloantibodies were detected respectively without cell-mediated immunity against liver antigen or lymphocytotoxic activity. Anti-liver, anti-DNA, anti-Ig and anti-lymphocyte antibodies were shown 6-7 weeks after the beginning of the infection concomitantly with the increase of immunoglobulin levels and circulating immune complexes. At this period, the antibody response to polyvinylpyrrolidone (PVP) was increased and the injection of spleen cells from day-45-infected mice to uninfected recipients increased the anti-PVP antibody response. Conversely, the injection of spleen cells from uninfected to infected mice did not modify the anti-PVP Ab response. After 6 weeks of infection, the basal thymidine incorporation of spleen cells was increased contrasting with the marked inhibition of spleen cell response to PHA. The present data are consistent with the induction of a polyclonal non-specific B cell activation by S. mansoni.

Animals↗