[Effect of ionized fields on the vitality and ratio of mutation of bacteria in suspension in the air].
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Biomedical subjects
Publications and source records attributed to R Fontanges.
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The immunomodulator OM-89 (bacterial extract from E. coli), known to act on the immune system by modulating both humoral and cellular responses, significantly increases ACTH and glucocorticoids secretion in normal Wistar rats. A comparative administration of IL-1 displays a similar pattern of release. Moreover, OM-89-induced responses are blocked by IL-1ra, the soluble receptor antagonist of IL-1. The effect of OM-89 can thus be explained, at least in part, via IL-1 which directly enhances the secretion of both stress hormones. Finally, a comparative experiment between control and stressed rats (by immobilization) shows that the responses to OM-89 measured in this study (ACTH and corticosterone secretion) are stress-modulated.
The trace elements are surrounding factors which are able to act on the yield of benzo(a)pyrene hydroxylation reaction of the hepatic tissue. This action was studied for each element and for various concentrations. The action of these elements may occurred to arylhydrocarbon hydroxylase by activating or inhibiting it, to epoxyde hydrase or to glutathione S epoxydase, favouring or inhibiting the way epoxyde dihydrodiol, and finally to arylhydrocarbon hydroxylase induction. Our results, obtained in vitro on hepatic tissue with many metallic salts, showed that some trace elements may have a cocarcinogenic action.
The immune response to Vibrio cholerae was studied in baboons, rhesus monkeys and marmosets inoculated by the oral, intraintestinal or intravenous route with various strains of V. cholerae. Sera were collected from all animals on days 2, 6, 10, 17, 24, 32, 45 and 60 after infection. Serum protein, immunoglobulins (IgA, IgG, IgM), GOT, and alkaline phosphatases were determined. The results showed that baboons and rhesus monkeys were not susceptible to cholera infection under these experimental conditions. However, we were able to induce a lethal cholera infection in cotton-topped marmosets. In baboons and rhesus monkeys serum IgG levels decreased significantly following inoculation with V. cholerae; however, the ratio of GOT, alkaline phosphatase and antibodies against toxin were only slightly modified.
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The authors reviewed the data about inflammatory diseases acquired in the last few years. They have studied clinical aspects of inflammatory reaction, the various mediators of inflammation and physiological anti-inflammatory molecules.
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In a previous chapter, the importance of macrophages in inflammatory processes was emphasized upon. The authors now mention the outstanding inflammatory agents utilized for experimental purposes, especially as regards the pattern of their action. Finally, this paper restates the question of the pharmacology and therapy in inflammation.
Four-week old BALB/c mice were fed a 4% protein diet for 6 weeks. At the 3rd week of undernourishment, they were orally vaccinated with a live vaccine, Salmonella typhimurium Rc. the mice were challenged 3 weeks after vaccination, and malnutrition was discontinued at that time. Results suggested that the live vaccine may be pathogenic when associated with a protein-deficient diet.
The variations in anti-Salmonella typhimurium antibody levels was measured in BALB/c mice which had been orally and nasally vaccinated with S. typhimurium live mutants of different lipopolysaccharide lengths. Together with the demonstration of immunological memory, the intensity of the secondary response was correlated with the length of the polysaccharide chain at intestinal and serum levels. Nasally administered antigen seemed to be at least as immunogenic as when orally administered.
Oral vaccination with Salmonella typhi-murium M 206 has been shown to confer highly significant protection on BALB/c and low-responder (LR) Biozzi mice a 30 days, but no protection was observed in high-responder (HR) Biozzi mice. None of the three strains showed any evidence of significant protection 10 days after primary vaccination. A correlation was noted between the degree of protection and the results of tests measuring cell-mediated immunity, both in vitro (MIF test), and in vivo (colloidal carbon clearance). Phagocytosis was significantly more active in vaccinated mice, both at days 10 and 30, except in HR mice. MIF production was only found at day 10 in HR mice, and was present at day 30 in both HR and LR mice. Our results emphasize the importance of the role of macrophage phagocytosis in the protection of mice against Salmonella infections.
Eleven calves, 6 months old, vaccinated or not, have been infected experimentally with 10(7) Salmonella typhi-murium, administered by oral route. The control calves had a serious illness, characterized by a severe diarrhoea, hepatic and renal symptoms and a heavy infestation of the main organs. The other five calves, which were orally and subcutaneously vaccinated with ribosomal extracts of S. typhi-murium and S. dublin showed only a moderate alteration of their health while biochemical disorders at the level of liver and kidneys disappeared. However, salmonella were found in mesenteric lymph nodes, but in much lower amounts than in controls.
The specific anti-LPS serum antibody response in BALB/c mice, before and after an oral booster with different non-pathogenic strains of Salmonella typhi-murium, was measured by an ELISA technique. Serum response to LPS was found to depend on the length of the LPS polysaccharide moiety in "rough" mutants. The M206 "smooth" mutant induced a less marked anti-LPS response. The immunogenicity of the polysaccharidic "core" appears to be modified by the O antigen. The specific antibody response in the gut only becomes marked following after booster of Ra, Rc and M206 mutants.