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Biomedical subjects

F Floc'h

Publications and source records attributed to F Floc'h.

31 records · Page 2Linked to original sources
PubMedDate not supplied

Immunostimulating substances from human casein.

Delipidated human casein was digested with trypsin and the enzymatic digest was fractionated on Sephadex G-50. The peptidic fractions were assayed for immunomodulating activity in two in vitro models. Fractions corresponding to molecular weights in the range of 2,000 +/- 600 were found to possess stimulating activity in these models.

Adjuvants, Immunologic↗
PubMedDate not supplied

Increased resistance to virus infections of mice inoculated with BCG (Bacillus calmette-guérin).

CD-1 or OF-1 mice were inoculated intravenously with 1 mg per mouse (i.e. about 10(6) live bacilli) of Pasteur Institute BCG and challenged 15 to 31 days later with the following viruses introduced by various routes: encephalomyocarditis, murine hepatitis, type 1 and 2 herpes simplex, foot-and-mouth disease and A0 and A2 influenza viruses. In most cases, BCG-inoculated mice exhibited a significantly higher resistance to these lethal infections than control mice (overall survival in control: 18%; in BCG-inoculated mice: 41%). Enhancement of resistance by BCG was especially marked in infections with encephalomyocarditis, herpes simplex type 1 and influenza A2 viruses. Intercurrent infection of BCG-inoculated mice with non lethal doses of viruses did not abrogate their resistance towards subsequent challenge with lethal doses of an unrelated virus. The possible mechanisms of this enhancing effect of BCG on host's resistance are discussed in the light of the known effects of this immunostimulating agent on the various facets of the immune response and of the respective roles the latter play in the defence against virus infections.

Animals↗
PubMedDate not supplied

RP 55778, a PAF receptor antagonist, prevents and reverses LPS-induced hemoconcentration and TNF release.

Platelet-activating factor (PAF) and tumor necrosis factor (TNF) are present in the plasma of animals injected with endotoxin (LPS). Furthermore, when exogenously administered to animals, PAF and TNF induce similar pathological effects. Thus, in order to explore a possible link between these two factors, the effects of a PAF receptor antagonist, RP 55778, and a glucocorticoid, dexamethasone, were studied on LPS-induced hemoconcentration in rats and on the release of TNF induced by exposing isolated murine macrophages to LPS. RP55778 administered either before or after LPS inhibited these endotoxin effects whereas dexamethasone was effective only when given prior to the LPS challenge. Additionally, in murine macrophages the strong TNF mRNA signal induced by LPS was abolished by RP 55778 and dexamethasone treatment. These results indicate that PAF and TNF can mediate the functional manifestations associated with endotoxemia and only RP 55778 appears to show potential for activity against an already established LPS response.

Animals↗
PubMedDate not supplied

Heterotypic protective immune reactions in mice infected with distinct serotypes of human influenza virus.

Infection of mice with subtype A0 OR A2 human influenza viruses, by a non-respiratory route causing no lethality, renders the animals markedly resistant to subsequent respiratory challenge with a strain differing from the first one through its haemagglutinin and neuraminidase antigens. This state of heterotypic immunity which appears rapidly (5 days) after the first infection, manifests itself during the second infection by a much reduced mortality, by less extensive lung lesions than in the control mice and by a final drop in lung virus titre (while in controls this titre stays at a high level until death) associated with a rapid rise of serum antibody levels against the haemagglutinin of the challenge virus and the "soluble" antigen common to type A strains. The development of this state of heterotypic immunity is dependent on the capacity of the first virus inoculated to replicate actively in the mouse. The role played by cell-mediated immunity in this phenomenon is evidenced by the fact that both the induction and the expression of this state of heterotypic resistance may be abolished by treatment of the mice with anti-thymocyte serum, while they are not affected by cyclophosphamide. Furthermore, in the mouse infected with an influenza A0 or A2 virus, it has been possible to demonstrate completely cross-reactive delayed type hypersensitivity reactions against the virions or their products. The fact that heterotypic immunity is not demonstrable between influenza viruses of type A and B favors the hypothesis that an antigen (matrix or nucleoprotein) common to all A subtypes--but different in B type strains--plays a role in these reactions of cross-protection.

Amantadine↗
PubMedDate not supplied

Comparative effects of an inflammatory reaction on the resistance of mice to bacterial and viral infections.

The induction in mice of a sterile subcutaneous granuloma exerted no influence upon the mortality following their infection with herpes type 1, murine hepatitis or encephalomyocarditis viruses. Attempts to reproduce the resistance -- which has been found to occur as a result of the granulomatous reaction, in the case of bacterial, fungal or protozoa infections and tumour invasions -- by varying the route and timing of the virus inoculation or the strain of mice have failed. We conclude that it is not merely through their inflammatory properties that some non-specific immunostimulating substances enhance resistance against viral infection.

Aging↗
PubMedDate not supplied

Inhibitory effect of interferon on DNA and RNA synthesis in murine spleen cells stimulated by lectins.

Spleen cells from mice inoculated with partially purified preparations of interferon (Sp. Act. 1 X 10(7) i.u./mg protein, 0.2 ml i. v./mouse) were stimulated in vitro with phytohemagglutinin, concanavalin A or lipopolysaccharide. After 2 days of stimulation, the incorporation of 3H-thymidine into TCA-insoluble radioactivity was inhibited 50-90% when compared with cells from animals inoculated with mock interferon. Maximal inhibition, with optimal doses of lectins was obtained when interferon was;inoculated 18 hours before. This effect of interferon on DNA synthesis was preceeded by inhibition of the incorporation of 3H-uridine into TCA-insoluble material. When cells were pretreated in vitro with interferon for 24 hours and subsequently stimulated with PHA, RNA synthesis was inhibited by 30-40%, whatever was the dose of the mitogen. The synthesis of 4S tRNA, 18S and 28S ribosomal RNAs were inhibited to the same degree by interferon. The incorporation of methyl groups into cytoplasmic sRNA was unaltered.

Animals↗