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Biomedical subjects

J Taverne

Publications and source records attributed to J Taverne.

At least 91 records · Page 5Linked to original sources
PubMed1986

A comparison of eosinophil-activating factor (EAF) with other monokines and lymphokines.

Monocytes from moderately eosinophilic individuals secrete material that enhances the cytotoxic activity of eosinophils against antibody-coated schistosomula of Schistosoma mansoni. This material is not a single substance, but can be fractionated into several active components of different size and different charge. Gel filtration of mononuclear cell supernatants separated the eosinophil-activating activity into a major component of molecular mass of 40 kDa and a minor component of molecular mass of less than 10 kDa. The major component exhibited further heterogeneity on fractionation by high performance liquid chromatography. The bulk of the eosinophil-activating activity could be separated from both colony-stimulating factor (CSF) alpha activity and from tumor necrosis factor (TNF) activity. However, human recombinant CSF alpha (GM-CSF), human recombinant TNF and rabbit tumor necrosis serum all had eosinophil-activating activity when tested against schistosomula. Eosinophils were not activated by interleukin 1, interleukin 2, interferon-alpha, lipopolysaccharide or phorbol myristate acetate.

Colony-Stimulating Factors↗
PubMed1986

Macrophage cytotoxicity in lethal and non-lethal murine malaria and the effect of vaccination.

We investigated the development of cell-mediated immunity in lethal and non-lethal malarial infections by assaying the cytotoxic activity of spleen cells for L929 tumour cells at different times after infection of mice with the lethal P. berghei, a lethal variant of Plasmodium yoelii and the non-lethal P. yoelii and P. chabaudi. In all cases the cytotoxicity increased to a peak during the first week and then diminished but the time of the peak varied with the infection; its activity was lowest with P. berghei. A second peak occurred in the non-lethal infections at the time of recovery. A protective vaccine accelerated and enhanced the early peak of cytotoxicity. The activity was mediated by adherent phagocytic cells, probably through the release of tumour necrosis factor (TNF) by macrophages since it was inhibited by antiserum against recombinant mouse TNF and did not destroy TNF-resistant L929 cells. Its induction was not dependent on T cells since it occurred in T cell-deficient mice infected with non-lethal P. yoelii. However, the accelerated increase associated with vaccination could be adoptively transferred by spleen lymphocytes from vaccinated mice.

Animals↗
PubMed1985

Macrophages as effector cells in immunity to malaria.

Experiments with malaria in mice suggest that protective immunity depends not only on antibody but also on activation of macrophages. Activated macrophages may cause intra-erythrocytic death of parasites by releasing reactive oxygen intermediates and/or tumour necrosis factor. Macrophage activation for both types of product correlates well with the timing of recovery in a range of different malaria infections and in mice protected by vaccination.

Animals↗
PubMed1985

Immunity to an attenuated variant of Plasmodium berghei: role of some non-specific factors.

Plasmodium berghei XAT, an attenuated variant of lethal P. berghei, causes a resolving infection in Balb/c mice from which they recover in about 3 weeks. The parasitaemia displays an early peak at about 5 days, followed by a steep drop in parasite number associated with the appearance of degenerating forms inside mature erythrocytes; the parasites remaining are inside reticulocytes. By contrast, no degenerating parasites were seen in infections caused by the virulent parent, which was mainly confined to mature erythrocytes. However, P. berghei XAT was no more sensitive to reactive O2 metabolites, generated by alloxan, or to tumour necrosis serum, than its virulent parent. Furthermore, its early drop in parasitaemia was unaffected by silica. The drop still occurred in the absence of T cells, although the infection was then ultimately lethal, and it was not mediated by NK cells since it occurred in nude mice treated with anti-asialo GM1 serum to abolish NK cell activity. However, it was absent in splenectomized mice, in which P. berghei XAT infection was lethal. Thus, the attenuation of P. berghei XAT infection is not due to increased susceptibility to some of the agents thought to cause parasite destruction, but to some other mechanism in which the spleen is involved.

Animals↗
PubMed1985

Macrophage functions in Biozzi mice.

The faster degradation of antigen by macrophages in Biozzi low (L) responder mice, compared to Biozzi high (H) responder mice, is thought to be responsible for their lower antibody response. We have measured four functions associated with macrophages to see whether macrophages from L mice were generally more active than those from H mice. Peritoneal macrophages obtained from normal mice were compared with those from groups of mice given Mycobacterium bovis BCG or Propionibacterium acnes. Cells from normal H mice gave a stronger oxidative burst when triggered with phorbol myristate acetate, and were more cytotoxic for tumour cells than cells from L mice. Cells from all mice injected with BCG or P. acnes gave a stronger oxidative burst, and were more cytotoxic for tumour cells; again, both responses were higher in H mice than in L mice. By contrast, when groups of mice that had received P. acnes were given endotoxin and bled, higher titres of tumour necrosis factor were found in the sera of L mice. Spleen cells from both lines of mice released similar levels of interleukin-1, both spontaneously and in response to lipopolysaccharide. Our results suggest that these various macrophage responses are expressed independently in H and L mice.

Animals↗
PubMed1984

Killing of human malaria parasites by macrophage secretory products.

The susceptibility of the human malaria parasite, Plasmodium falciparum, to killing in vitro by macrophage secretory products was investigated. The effect of O2 radicals and tumor necrosis factor on parasite viability was assessed both morphologically and by following the uptake of [3H]hypoxanthine. H2O2 produced by the interaction of glucose and glucose oxidase was found to reduce viability; this effect was reversed by the addition of exogenous catalase. Further studies indicated that the catalase level within the erythrocyte was not altered upon parasite invasion. O2 radicals produced during the xanthine-xanthine oxidase interaction also killed P. falciparum. The addition of various O2 radical scavengers (including catalase) did not reverse this effect; therefore, it was not possible to determine which of the O2 radicals were involved in the killing process. Samples from three different sources containing tumor necrosis factor, a nonspecific soluble mediator derived from Mycobacterium bovis BCG-activated macrophages treated with endotoxin, also killed the parasite. There was no evidence that tumor necrosis factor or the products of the xanthine-xanthine oxidase interaction caused damage to the erythrocyte membrane that could be implicated as an important aspect of the killing process. These findings all strongly suggest that such macrophage products play an important role in immunity to malaria.

Animals↗
PubMed1984

Malarial parasites and tumour cells are killed by the same component of tumour necrosis serum.

Tumour necrosis serum (TNS), from animals primed with macrophage activating agents and challenged with endotoxin, causes necrosis of some tumours and can kill certain tumour lines in vitro and malarial parasites in vitro and in vivo. We have tested the possibility that the same factor is responsible for killing both tumour cells and malarial parasites. In competitive inhibition experiments, parasitized erythrocytes, but not normal erythrocytes, inhibited the cytotoxicity of TNS against a tumour cell line. Conversely, the tumour cells inhibited the killing of Plasmodium yoelii in vitro by TNS. When rabbit TNS was fractionated by ion exchange chromatography followed by gel filtration and the fractions at each step were pooled according to their ability to kill the tumour cells, in vitro parasite killing activity was found to correlate with tumour cell cytotoxicity, to a final sample which was purified more than 600-fold. Our results suggest that in terms of function, at least, the same component of TNS is responsible for the killing of both tumour cells and malarial parasites.

Animals↗
PubMed1982

Killing of the malarial parasite Plasmodium yoelii in vitro by cells of myeloid origin.

Cytotoxic effects of mouse cells on Plasmodium yoelii were sought directly by incubating parasitized red cells with cells of various kinds for 16 h and then determining the percentage parasite survival in vivo, in terms of infectivity for the mouse. Cell populations rich in lymphocytes, e.g. lymph node and spleen, were less active than peritoneal cells and blood. Parasite killing by peritoneal cells was associated with macrophages: treatment with anti-macrophage serum (AMS) or depletion by adherence or centrifugation on Ficoll decreased activity. Polymorphonuclear leucocytes (PMN) in induced exudates may have contributed to killing, although not as actively cell for cell, and an effect of eosinophils in worm-induced exudates was not excluded. White blood cells were most active of all and fractionation on Ficoll confirmed that lymphocytes were relatively ineffective. The effector cell was phagocytic but it was insensitive to AMS. Tests on populations wih high or low proportions of PMN showed that parasite killing was independent of PMN number. It is concluded that the effector cell belongs to the monocyte-macrophage series and has acquired the ability to kill the parasite before becoming fully differentiated into a macrophage.

Animals↗
PubMed1982

Differential sensitivity in vivo of lethal and nonlethal malarial parasites to endotoxin-induced serum factor.

Sera from mice infected with Plasmodium yoelii or Plasmodium berghei and given endotoxin contained nonspecific mediators which killed both species of parasite and tumor cells in vitro. The sera resembled tumor necrosis sera obtained from mice given macrophage-activating agents such as Propionibacterium acnes (formerly designated Corynebacterium acnes) or Mycobacterium bovis BCG and then endotoxin. Cytotoxicity developed parallel to parasite killing activity and indicated that macrophages were activated. Activation occurred sooner with P. berghei, which is lethal, and serum activity remained on a plateau until the mice died. In nonlethal P. yoelii infections, activation was related to the course of parasitemia. Endotoxin given to mice infected with P. yoelii caused an immediate decrease in parasitemia, presumably through the release of parasite killing factors. The extent of the decrease depended upon the time of administration. No immediate drop in the parasitemia caused by P. berghei was observed at any time. Early administration of endotoxin prolonged survival; late administration accelerated death. Passive transfer of rabbit tumor necrosis serum to infected mice decreased the parasitemia caused by P. yoelii but not that caused by P. berghei. Other components of the immune response appeared to act together with these soluble mediators to eliminate P. yoelii; they may be absent or suppressed in infections with P. berghei.

Animals↗
PubMed1981

Endotoxin-induced serum factor kills malarial parasites in vitro.

We investigated the possibility that malarial parasites may be killed by nonspecific soluble mediators, such as those in tumor necrosis serum, that are obtained from mice given macrophage-activating agents like Corynebacterium parvum or Mycobacterium bovis BCG, followed by endotoxin. Such sera killed parasites in vitro after overnight incubation; killing was measured directly by using an in vivo infectivity assay. Parasite infectivity was not decreased by incubation in sera from mice given C. parvum or BCG alone (no endotoxin) or by incubation in sera from normal mice given endotoxin. Plasmodium yoelii, its lethal variant, and Plasmodium berghei were equally susceptible to inactivation. Sera obtained from mice given endotoxin during the course of infection with these parasites also contained parasite-killing factor. The activity of this factor appeared to be proportional to parasitemia in that it was higher in the sera from mice infected with the lethal parasites than in the sera from mice with infections which resolved either spontaneously or after vaccination.

Animals↗
PubMed1979

Cell-mediated immunity in the liver of mice vaccinated against malaria.

Mice can be protected against several species of lethal malaria infection by vaccination, and their recovery correlates well with increased anti-malarial antibody levels, particularly IgG (ref.2). However, there is also a good correlation between protection by vaccines and priming for delayed-type hypersensitivity in the skin, although there is no obvious explanation for this effect. We now report an apparent relationship between protection and a cell-mediated immune response involving the migration of various types of cell capable of killing malaria parasites in vitro to the liver. We suggest that the effect of vaccination is to bring together parasites, specific antibody and nonspecific cytotoxic cells, and that the liver may be a major site for their interaction.

Animals↗
PubMed1979

Development and suppression of a population of late-adhering macrophages in mouse malaria.

Changes in phagocytic and adherent cell numbers were compared during the course of infections of mice with Plasmodium yoelii (Py) and P. berghei (Pb) and in vaccinated mice challenged with homologous parasites. Nucleated cells in the spleen increased in number in Py-infected mice and were maximal at the time of recovery. The number of phagocytic cells increased in parallel, as did the number of blood leucocytes. Rates of increase were accelerated in vaccinated mice. Changes in Pb-infected mice resembled controls and blood leucocytes showed no consistent increase. In infected mice, the number of spleen and bone marrow cells which adhered to plastic rose above normal. At some stages of infection, cells which did not adhere in 24 h did so in 72 h. Such late-adhering cells, which resembled macrophages in morphology, were most numerous at the time of recovery. They appeared to be derived from monocyte precursors which matured in culture. Sometimes cells adherent at 24 h suppressed the development of the late-adhering population. Silica invactivated these suppressive macrophages but did not affect the precursors which developed into late-adhering cells. It is concluded that malarial infection stimulates the production of precursors of the macrophage-monocyte series and that their development is regulated by the presence of mature macrophages.

Animals↗
PubMed1976

Detection of immune complexes in mice infected with Mycobacterium lepraemurium.

A specific binding test was used to detect immune complexes containing antigens of Mycobacterium lepraemurium in the serum and tissues of infected mice. Complexes were precipitated by antiserum against immunoglogulin, free antigen removed by washing and the presence of bound antigen demonstrated by measurement of uptake of radioactively labelled specific antibody by the precipitate. Tests were done both with 125I-labelled FAB prepared from an immune from rabbit antiserum against M. Lepraemurium and with 125I-labelled IgG precipitate. Out of seventy-nine serum samples taken monthly up to the 5th month after infection, only there were positive (one at 2 months and two at 3 months). Kidneys taken from infected mice were also examined for immune complexes. Although deposits of IgM and sometimes of IgG were observed by immunoflourescence in glomeruli of normal mice, deposits of IgG were more frequent later on in infected mice. Nevertheless, binding tests done on acid eluates were positive in only one out of fifty-three infected mice.

Animals↗
PubMed1974

Cultivation of TRIC agents: a comparison between the use of BHK-21 and irradiated McCoy cells.

BHK-21 cells and HeLa cells were as sensitive as irradiated McCoy cells for titrating both fast- and slow-growing strains of TRIC agents. BHK-21 cells were as efficient as irradiated McCoy cells for isolating TRIC agents from trachoma and from the genital tract of patients with non-gonococcal urethritis. More inclusions were formed in BHK-21 than in irradiated McCoy cells.

Animals↗
PubMed1974

Neutralization of TRIC organisms by antibody: enhancement by antisera prepared against immunoglobulins.

The neutralizing activities of fowl, rabbit and mouse antisera prepared against TRIC agents were enhanced, in some cases over a 100-fold, by the addition of antiserum against the appropriate IgG. Significant non-specific inactivation of the organisms was observed in the absence of antiserum against TRIC agents, in reaction mixtures containing normal serum and antiserum against IgG. Since the extent of this inactivation showed a prozone, control tests with dilutions of normal serum equivalent to the full range of dilutions of the antiserum tested are necessary to show that enhancement of neutralization is specific.

Animals↗
PubMed1974

Interactions of TRIC agents with macrophages: effects on lysosomal enzymes of the cell.

TWO CHANGES WERE OBSERVED IN THE ACID PHOSPHATASE OF MACROPHAGES THAT HAD INGESTED INFECTIVE TRIC ORGANISMS: the proportion of extralysosomal enzyme rose, while the total amount in the cells fell. Both effects were directly related to the number of organisms ingested and increased with time. When macrophages were inoculated with more than 50 organisms per cell, changes were obvious within a few hours; with 2-10 organisms per cell changes were detectable only after 18 hr. or more. Enzyme appeared in the culture medium as the amount in the cells decreased. Ingestion of organisms killed by heat or treated with antibody did not induce such changes. In infected BHK-21 cells, no changes in acid phosphatase were detected at any stage of the developmental cycle of the organism.

Acid Phosphatase↗