Nippon Saikingaku Zasshi
Online ISSN : 1882-4110
Print ISSN : 0021-4930
ISSN-L : 0021-4930
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Volume 43, Issue 4
Displaying 1-9 of 9 articles from this issue
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  • Virulence factor of Legionella pneumophila
    Kohei HARA
    1988 Volume 43 Issue 4 Pages 799-807
    Published: July 25, 1988
    Released on J-STAGE: February 19, 2009
    DOIhttps://doi.org/10.3412/jsb.43.799
    JOURNAL FREE ACCESS
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  • Changing pattern of respiratory pathogens due to development of antibacterial agents
    Keizo MATSUMOTO
    1988 Volume 43 Issue 4 Pages 809-820
    Published: July 25, 1988
    Released on J-STAGE: February 19, 2009
    DOIhttps://doi.org/10.3412/jsb.43.809
    JOURNAL FREE ACCESS
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  • Heat-killed Lactobacillus casei, LC-9018, as an interferon inducer
    Fujio SUZUKI, Hiroaki OKABE, Takeomi TODAKA, Keiko HAYASHI, Fusaoki KO ...
    1988 Volume 43 Issue 4 Pages 821-827
    Published: July 25, 1988
    Released on J-STAGE: February 19, 2009
    DOIhttps://doi.org/10.3412/jsb.43.821
    JOURNAL FREE ACCESS
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    A viral inhibitory activity was found in sera of ddY mice treated intraperitoneally with heat-killeld Lactobacillus casei LC-9018, at doses of 0.78-200mg/kg. The activity was ascribed to interferon(s) (IFN). A significant IFN activity of the sera of mice appeared in 18 hours and it reached a peak between 18-24 hours after the stimulation. In vitro treatment with anti-IFNγ antiserum neutrarized 67% of the IFN activity. The IFN-inducing activity of LC-9018 was diminished when mice were pretreated with monoclonal anti-Thy1, 2 antibody or carrageenan. These results suggest that T-cells and macrophages may be required for IFN induction with LC-9018.
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  • Prevention of Experimental Antibiotic-Associated Diarrhea by Clostridium butyricum
    Nobuhiro TAGUCHI, Fumihiko ABE, Yuzuru MIKAMI, Tadashi ARAI
    1988 Volume 43 Issue 4 Pages 829-835
    Published: July 25, 1988
    Released on J-STAGE: February 19, 2009
    DOIhttps://doi.org/10.3412/jsb.43.829
    JOURNAL FREE ACCESS
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    A golden-hamster model of antimicrobial agent-associated lethal enterocolitis was produced by oral administration of cef atrizine (CFT). In all diarrheal and dead animals, the striking finding at necropsy was enterocolitis in which the cecum and distal ileum were greatly distended with fluid: toxigenic Clostridium difficile was detected at 108 CFU/head or greater. Bacteria-free cecal filtrate and culture filtrate of C. difficile isolated from the cecal contents of diarrheal animals exhibited lethal toxicity to normal hamsters. A single oral administration of CFT (75mg/kg) produced lethal enterocolitis in 17 of 20 animals during a one-month period of observation.
    Clostridium butyricum Miyairi (CbM), spores, used as an enteroregulator, were investigated for their potential to prevent the lethal enterocolitis in this model. Animals were administrated CbM orally (109 CFU/day) for three consecutive days after CFT challenge, and this prevented death in 16 of 20 animals during one mouth of observation. These results suggest that CbM has a preventive effect against lethal enterocolitis in this model.
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  • Inhibitory effect of lipopolysaccharides, natural lipid A and synthetic lipid A on growth of murine B cell lines, CYG 34 and CYG 101
    Fumiko HONDA, Teruo KIRIKAE, Masao YOSHIDA, Kanji ISHIBASHI, Kazuhito ...
    1988 Volume 43 Issue 4 Pages 837-843
    Published: July 25, 1988
    Released on J-STAGE: February 19, 2009
    DOIhttps://doi.org/10.3412/jsb.43.837
    JOURNAL FREE ACCESS
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    Re-mutant lipopolysaccharide (Re LPS) of Salmonella minnesota profoundly inhibited the growth of murine B-cell lines, designated CYG34 and CYG101, established from long term bone-marrow culture. When CYG101 cells were cultured together with Re LPS at concentrations of 2-100μg/ml, the cell proliferation was dose-dependently suppressed. Re LPS hardly or slightly affected the growth of a murine T-cell line, BW5147, pre-B cell lines, 70Z/3 and CYG 8, and a myeloma cell line, X63Ag8. S-form LPS of Escherichia coli and S. typhimurium, Re-mutant LPS of S. minnesota and natural lipid A of E. coil, S. typhimurium and S. minnesota also inhibited the growth of CYG101 cells. However, degraded polysaccharide of S-form LPS of S. typhimurium did not inhibit the cell growth. Synthetic compounds 406, corresponding to a biosynthetic disaccharide lipid A precursor, and 506, corresponding to lipid A of the E. coli type, also inhibited the growth of CYG101 cells. These results suggest that the growth inhibition of cell lines by LPS is selective or specific to the cell line and that the lipid A portion of LPS is involved in this growth inhibition. Double acyl groups of lipid A may not play any role in the inhibition of cell growth.
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  • [title in Japanese]
    1988 Volume 43 Issue 4 Pages 845-855
    Published: July 25, 1988
    Released on J-STAGE: February 19, 2009
    DOIhttps://doi.org/10.3412/jsb.43.845
    JOURNAL FREE ACCESS
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  • [title in Japanese]
    1988 Volume 43 Issue 4 Pages 856-873
    Published: July 25, 1988
    Released on J-STAGE: February 19, 2009
    DOIhttps://doi.org/10.3412/jsb.43.856
    JOURNAL FREE ACCESS
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  • [title in Japanese]
    1988 Volume 43 Issue 4 Pages 874-885
    Published: July 25, 1988
    Released on J-STAGE: February 19, 2009
    DOIhttps://doi.org/10.3412/jsb.43.874
    JOURNAL FREE ACCESS
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  • Erratum
    1988 Volume 43 Issue 4 Pages 892
    Published: 1988
    Released on J-STAGE: February 19, 2009
    DOIhttps://doi.org/10.3412/jsb.43.4_892
    JOURNAL FREE ACCESS
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