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Biomedical subjects

R Pautrizel

Publications and source records attributed to R Pautrizel.

At least 19 recordsLinked to original sources
PubMed1982

The variable surface glycoproteins of Trypanosoma equiperdum are phosphorylated.

The phosphoproteins from three Trypanosoma equiperdum variants were studied by labelling the parasites in vivo with 32P. Phosphoprotein analysis reveals the presence of a 58 000 mol. wt. phosphoprotein ( pp58 ) which is absent when live trypanosomes are pre-treated with proteinase K under conditions where only the surface coat containing the variable surface glycoprotein (VSG) is removed. Immunological and fingerprint analysis on labelled pp58 , purified from these variants by affinity chromatography on Concanavalin A-Sepharose, clearly identify this component as the VSG. Furthermore, the VSGs seem to be phosphorylated to the extent of 1 mol phosphate per mol glycoprotein. The phosphorylated region is located in the extreme C-terminal region representing approximately 10% of the total molecule. The phosphorylated residue is not an aliphatic or aromatic ester of serine, threonine, or tyrosine, nor an acyl phosphate involving an aspartyl or glutamyl residue, nor phosphohistidine. The evidence that VSGs are phosphorylated could have considerable implications for the transfer and function of these structures.

Animals↗
PubMed1981

Immune depression and macroglobulinemia in experimental subchronic trypanosomiasis.

The effects of subchronic trypanosomiasis upon immune responses were examined in Trypanosoma gambiense infection and in subcurative treatment of T. brucei- and T- equiperdum-infected mice. About 60% of the mice infected with T. gambiense developed a subchronic infection similar to human trypanosomiasis, characterized by the absence of circulating trypanosomes. The animals died between 1 and 12 months after infection with elevated serum immunoglobulin M (IgM) levels (16 times the normal level). After 1 month of infection, the mice showed a normal primary antibody response against sheep erythrocytes, as tested by hemagglutination, despite their high serum IgM levels. After more than 1 month of infection, about 20% of the mice showed depressed hemagglutination titers (25% of control), whereas all relapsed mice that contained circulating parasites showed a pronounced suppression. Elimination of the blood parasites with Berenil treatment restored immune competence, which persisted until the relapse of the animals. Identical results were obtained in T. brucei-infected mice. Berenil treatment abolished the immune depression against sheep erythrocytes, but did not cure the animals, which relapsed with the development of a new state of immune depression. T. gambiense and T. brucei infections were always followed by a marked increase of serum IgM levels. Hypergammaglobulinemia was also induced in relapsing T. equiperdum-infected mice treated with Berenil. No immune depression against sheep erythrocytes could be detected. It appeared that immune depression was not the result of clonal exhaustion (measured by the serum IgM level) but seemed to be closely associated with the presence of living trypanosomes.

Animals↗
PubMed1981

Macrophage function during Trypanosoma musculi infection in mice.

Quantitative and functional changes in peritoneal macrophages from mice infected with Trypanosoma musculi were investigated. Increase in the number and size and in the protein content of peritoneal macrophages and the presence of parasites in the peritoneal activity were observed during the course of parasitemia. Induced releases of H2O2 by macrophages were increased during parasitemia, but H2O2 release returned to normal after infection. A correlation was also observed between parasitemia and 99mTc colloidal uptake by peritoneal macrophages. These changes in macrophage function may indicate an activation of these cells.

Animals↗
PubMed1980

Absence of kinetoplast DNA in a late antigenic variant of Trypanosoma equiperdum.

We have analysed by several biochemical techniques the DNA components of two antigenic variants isolated from Trypanosoma equiperdum. We did not observe any kinetoplast DNA (kDNA) structures or networks in the late antigen variant BoTat 28. Furthermore, the results of reassociation kinetics of in vitro labelled kDNA show that neither kDNA minicircle sequences nor kDNA maxicircle sequences of BoTat 1, the basic antigen type, can be detected in the total DNA of BoTat 28.

Animals↗
PubMed1980

Anti-immunoglobulins and heterophil agglutinins in experimental trypanosomiasis.

Rheumatoid factor (RF)-like substances and heterophil agglutinins (HA) were induced in rabbits by infection with a strain of Trypanosoma equiperdum. Infection with a T. gambiense strain produced HA, but no RF. RFs appeared usually before immunoglobulin G (IgG) levels started to increase. They disappeared spontaneously after 4 to 6 weeks. HA were of the IgM class, appeared within 1 to 2 weeks after infection, and usually remained at high levels afterwards. They could not be absorbed out with lyophilized whole trypanosomes. Therapy suppressed the formation of RF as well as of HA, but IgG complexes as well as antibodies against trypanosomal antigens remained present for considerable periods after the installment of therapy. It is concluded that RFs are not induced by IgG complexes. The results suggest that HA are probably not cross-reacting antibodies induced by trypanosomal antigens.

Agglutinins↗
PubMed1978

[Changes in Plasmodium berghei berghei in mice maintained at high temperatures].

The study of the evolution of Plasmodium berghei berghei is made in mice kept in a high temperature (35 degrees C) throughout the experiment. Some of these mouse parasites (less than 30%) show a gigantic atypical morphology. In the parasite growing in animals kept at 35 degrees C, the amount of DNA is higher than DNA rate of the parasites growing in control mice (20-22 degrees C). There is no evidence of any relation between the increase of DNA amount and the morphological modification of these parasites.

Animals↗
PubMed1978

[Influence of a hot environmental temperature on the evolution of experimental paludism of the mouse with Plasmodium berghei berghei].

Swiss Mice infected with Plasmodium berghei berghei and maintained in permanence in a hot environmental temperature undergo a chronic infection whereas controls maintained at the laboratory temperature develop always an acute and lethal infection. The hot environmental temperature does not seem to have any action on the pathogenicity of the parasites. Host defences are stimulated.

Animals↗
PubMed1975

[Stimulation of the defenses of trypanosomic mice by a combination of magnetic field and electromagnetic wave radiation].

The remarkable efficiency of the physical treatment using such an association enables the mice to handle an infection otherwise lethal in a few days. The recovery is due to a very strong stimulation of defense system of the host-animal particularly those related to the immune responses. This effect can be obtained in spite of the depression of the immunological defenses prior to the infection. The control of the infection by the mice is not due to direct action of the radiation on trypanosomes.

Animals↗