Antitumoral effects of Pseudomonas aeruginosa lectins on Lewis lung carcinoma cells cultured in vitro without and with murine splenocytes

Dody Avichezer, Nechama Gilboa-Garber

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    11 Scopus citations

    Abstract

    Examination of the in vitro effects of PA-I and PA-II lectins of Pseudomonas aeruginosa on Lewis lung carcinoma cells revealed that these lectins differ in their effects. PA-I, the galactophilic lectin, exhibited both cytotoxic and cytostatic activities on these cells (tested by [3H]thymidine incorporation and by crystal violet vital staining). The two activities were dose and time dependent and inhibitable by the addition of methyl-α-d-galactoside to the culture medium. PA-II, the l-fucose and d-mannose binding lectin of the same Pseudomonas strain did not exhibit such a direct toxic effect on the tumor cells but affected them in the presence of splenocytes. Its addition to the tumor cells cocultured with murine (C57B1) splenocytes led to a profound cytolysis of the tumor cells, an effect which was inhibited by l-fucose.

    Original languageEnglish
    Pages (from-to)1305-1313
    Number of pages9
    JournalToxicon
    Volume29
    Issue number11
    DOIs
    StatePublished - 1991

    Bibliographical note

    Funding Information:
    The antitumoral activity of P. aeruginosa lectins, which act like toxins against cancer cells, is associated in the bacterium with a series of highly potent exocellular toxins (CRYZ, 1984), and intracellular toxins such as the cytotoxin/leukocidin (SCHARMANN, 1976; LuTZ, 1979) which are toxic for granulocytes (BwLTCH et al., 1985) and other normal and malignant cells ($ASAKI and LuTZ, 1985 ; LuTZ et al., 1987; KLUFTINGER et al., 1989) . The lectins and the latter toxins were localized in the periplasmic space of P. aeruginosa (GL1CK and GwRBER, 1983 ; KLUFITNGER et al., 1989) . However, whereas most of the above virulence factors are highly lethal for mice (LuTZ, 1979), PA-I and PA-II, up to 100 ~g/mouse, led to a marked increase in the spleen mass and lymphoid organs (AVICHEZER and Gn.BOw-GwRBSR, 1990) without lethality . The differential effects of the two Pseudomonas lectin preparations (PA-II, in contrast to PA-I, had no direct cytotoxic effect, but stimulated marine splenocytes) and their different sensitivity to inhibition by specific sugars confirmed their involvement in the antitumoral effect. Acknowledgements-This study was supported by the Mitzi-Dobrin Cancer Research Fund, Bar-Ilan University. The authors thank Mrs AvtttLt.e Goi.nxetctt for typing the manuscript and Mrs Etu Guvnt and Mrs Tessnn Axxrx for their help in the graphic and photographic representation of the work .

    Funding

    The antitumoral activity of P. aeruginosa lectins, which act like toxins against cancer cells, is associated in the bacterium with a series of highly potent exocellular toxins (CRYZ, 1984), and intracellular toxins such as the cytotoxin/leukocidin (SCHARMANN, 1976; LuTZ, 1979) which are toxic for granulocytes (BwLTCH et al., 1985) and other normal and malignant cells ($ASAKI and LuTZ, 1985 ; LuTZ et al., 1987; KLUFTINGER et al., 1989) . The lectins and the latter toxins were localized in the periplasmic space of P. aeruginosa (GL1CK and GwRBER, 1983 ; KLUFITNGER et al., 1989) . However, whereas most of the above virulence factors are highly lethal for mice (LuTZ, 1979), PA-I and PA-II, up to 100 ~g/mouse, led to a marked increase in the spleen mass and lymphoid organs (AVICHEZER and Gn.BOw-GwRBSR, 1990) without lethality . The differential effects of the two Pseudomonas lectin preparations (PA-II, in contrast to PA-I, had no direct cytotoxic effect, but stimulated marine splenocytes) and their different sensitivity to inhibition by specific sugars confirmed their involvement in the antitumoral effect. Acknowledgements-This study was supported by the Mitzi-Dobrin Cancer Research Fund, Bar-Ilan University. The authors thank Mrs AvtttLt.e Goi.nxetctt for typing the manuscript and Mrs Etu Guvnt and Mrs Tessnn Axxrx for their help in the graphic and photographic representation of the work .

    FundersFunder number
    Mitzi-Dobrin Cancer Research Fund
    Bar-Ilan University

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