Protective effect of granulocyte colony-stimulating factor against T- cell-meditated lethal shock triggered by superantigens

Y. Aoki, K. Hiromatsu, N. Kobayashi, T. Hotta, H. Saito, H. Igarashi, Y. Niho, Yasunobu Yoshikai

    Research output: Contribution to journalArticle

    28 Citations (Scopus)

    Abstract

    The bacterial superantigens (SAg), toxic shock syndrome toxin-1 (TSST-1) and staphylococcal enterotoxin B (SEB), are powerful T-cell stimulators, triggering systemic release of lymphokines causing lethal shock in D- galactosamine (D-Gal)-sensitized mice. We show that pretreatment with recombinant human granulocyte colony-stimulating factor (rhG-CSF) protects mice against T-cell-mediated SAg-shock. In mice challenged with D-Gal/TSST- 1, lethal shock was caused within 30 hours. In contrast, animals pretreated with two consecutive subcutaneous injections of 2 μg rhG-CSF with a 12-hour time interval showed only marginal signs of illness and no lethality after challenge with D-Gal/TSST-1. Mice treated with 5 μg rhG-CSF either 12 or 6 hours in advance also survived otherwise lethal doses of D-Gal/TSST-1. The protective effects of rhG-CSF pretreatment was also evident against lethal doses of D-Gal/SEB challenge and this protection was accompanied by suppression of systemic interleukin-2. However, rhG-CSF affected neither the proliferative responses of SAg-reactive T cells in vivo or in vitro nor their interleukin-2 production in vitro, implying that rhG-CSF may indirectly interfere with cytokine synthesis in T cells but not with T-cell-SAg binding itself. These results represent another beneficial effect of rhG-CSF as an antiinflammatory agent against T-cell-mediated toxicity triggered by SAg.

    Original languageEnglish
    Pages (from-to)1420-1427
    Number of pages8
    JournalBlood
    Volume86
    Issue number4
    Publication statusPublished - Jan 1 1995

    Fingerprint

    Superantigens
    T-cells
    Granulocyte Colony-Stimulating Factor
    Galactosamine
    Shock
    T-Lymphocytes
    Interleukin-2
    Lymphokines
    Subcutaneous Injections
    Toxicity
    Animals
    Anti-Inflammatory Agents
    Cytokines
    Staphylococcal enterotoxin F

    All Science Journal Classification (ASJC) codes

    • Biochemistry
    • Immunology
    • Hematology
    • Cell Biology

    Cite this

    Aoki, Y., Hiromatsu, K., Kobayashi, N., Hotta, T., Saito, H., Igarashi, H., ... Yoshikai, Y. (1995). Protective effect of granulocyte colony-stimulating factor against T- cell-meditated lethal shock triggered by superantigens. Blood, 86(4), 1420-1427.

    Protective effect of granulocyte colony-stimulating factor against T- cell-meditated lethal shock triggered by superantigens. / Aoki, Y.; Hiromatsu, K.; Kobayashi, N.; Hotta, T.; Saito, H.; Igarashi, H.; Niho, Y.; Yoshikai, Yasunobu.

    In: Blood, Vol. 86, No. 4, 01.01.1995, p. 1420-1427.

    Research output: Contribution to journalArticle

    Aoki, Y, Hiromatsu, K, Kobayashi, N, Hotta, T, Saito, H, Igarashi, H, Niho, Y & Yoshikai, Y 1995, 'Protective effect of granulocyte colony-stimulating factor against T- cell-meditated lethal shock triggered by superantigens', Blood, vol. 86, no. 4, pp. 1420-1427.
    Aoki Y, Hiromatsu K, Kobayashi N, Hotta T, Saito H, Igarashi H et al. Protective effect of granulocyte colony-stimulating factor against T- cell-meditated lethal shock triggered by superantigens. Blood. 1995 Jan 1;86(4):1420-1427.
    Aoki, Y. ; Hiromatsu, K. ; Kobayashi, N. ; Hotta, T. ; Saito, H. ; Igarashi, H. ; Niho, Y. ; Yoshikai, Yasunobu. / Protective effect of granulocyte colony-stimulating factor against T- cell-meditated lethal shock triggered by superantigens. In: Blood. 1995 ; Vol. 86, No. 4. pp. 1420-1427.
    @article{5b4f20a4ddc64089a94ebc7f934b4e8d,
    title = "Protective effect of granulocyte colony-stimulating factor against T- cell-meditated lethal shock triggered by superantigens",
    abstract = "The bacterial superantigens (SAg), toxic shock syndrome toxin-1 (TSST-1) and staphylococcal enterotoxin B (SEB), are powerful T-cell stimulators, triggering systemic release of lymphokines causing lethal shock in D- galactosamine (D-Gal)-sensitized mice. We show that pretreatment with recombinant human granulocyte colony-stimulating factor (rhG-CSF) protects mice against T-cell-mediated SAg-shock. In mice challenged with D-Gal/TSST- 1, lethal shock was caused within 30 hours. In contrast, animals pretreated with two consecutive subcutaneous injections of 2 μg rhG-CSF with a 12-hour time interval showed only marginal signs of illness and no lethality after challenge with D-Gal/TSST-1. Mice treated with 5 μg rhG-CSF either 12 or 6 hours in advance also survived otherwise lethal doses of D-Gal/TSST-1. The protective effects of rhG-CSF pretreatment was also evident against lethal doses of D-Gal/SEB challenge and this protection was accompanied by suppression of systemic interleukin-2. However, rhG-CSF affected neither the proliferative responses of SAg-reactive T cells in vivo or in vitro nor their interleukin-2 production in vitro, implying that rhG-CSF may indirectly interfere with cytokine synthesis in T cells but not with T-cell-SAg binding itself. These results represent another beneficial effect of rhG-CSF as an antiinflammatory agent against T-cell-mediated toxicity triggered by SAg.",
    author = "Y. Aoki and K. Hiromatsu and N. Kobayashi and T. Hotta and H. Saito and H. Igarashi and Y. Niho and Yasunobu Yoshikai",
    year = "1995",
    month = "1",
    day = "1",
    language = "English",
    volume = "86",
    pages = "1420--1427",
    journal = "Blood",
    issn = "0006-4971",
    publisher = "American Society of Hematology",
    number = "4",

    }

    TY - JOUR

    T1 - Protective effect of granulocyte colony-stimulating factor against T- cell-meditated lethal shock triggered by superantigens

    AU - Aoki, Y.

    AU - Hiromatsu, K.

    AU - Kobayashi, N.

    AU - Hotta, T.

    AU - Saito, H.

    AU - Igarashi, H.

    AU - Niho, Y.

    AU - Yoshikai, Yasunobu

    PY - 1995/1/1

    Y1 - 1995/1/1

    N2 - The bacterial superantigens (SAg), toxic shock syndrome toxin-1 (TSST-1) and staphylococcal enterotoxin B (SEB), are powerful T-cell stimulators, triggering systemic release of lymphokines causing lethal shock in D- galactosamine (D-Gal)-sensitized mice. We show that pretreatment with recombinant human granulocyte colony-stimulating factor (rhG-CSF) protects mice against T-cell-mediated SAg-shock. In mice challenged with D-Gal/TSST- 1, lethal shock was caused within 30 hours. In contrast, animals pretreated with two consecutive subcutaneous injections of 2 μg rhG-CSF with a 12-hour time interval showed only marginal signs of illness and no lethality after challenge with D-Gal/TSST-1. Mice treated with 5 μg rhG-CSF either 12 or 6 hours in advance also survived otherwise lethal doses of D-Gal/TSST-1. The protective effects of rhG-CSF pretreatment was also evident against lethal doses of D-Gal/SEB challenge and this protection was accompanied by suppression of systemic interleukin-2. However, rhG-CSF affected neither the proliferative responses of SAg-reactive T cells in vivo or in vitro nor their interleukin-2 production in vitro, implying that rhG-CSF may indirectly interfere with cytokine synthesis in T cells but not with T-cell-SAg binding itself. These results represent another beneficial effect of rhG-CSF as an antiinflammatory agent against T-cell-mediated toxicity triggered by SAg.

    AB - The bacterial superantigens (SAg), toxic shock syndrome toxin-1 (TSST-1) and staphylococcal enterotoxin B (SEB), are powerful T-cell stimulators, triggering systemic release of lymphokines causing lethal shock in D- galactosamine (D-Gal)-sensitized mice. We show that pretreatment with recombinant human granulocyte colony-stimulating factor (rhG-CSF) protects mice against T-cell-mediated SAg-shock. In mice challenged with D-Gal/TSST- 1, lethal shock was caused within 30 hours. In contrast, animals pretreated with two consecutive subcutaneous injections of 2 μg rhG-CSF with a 12-hour time interval showed only marginal signs of illness and no lethality after challenge with D-Gal/TSST-1. Mice treated with 5 μg rhG-CSF either 12 or 6 hours in advance also survived otherwise lethal doses of D-Gal/TSST-1. The protective effects of rhG-CSF pretreatment was also evident against lethal doses of D-Gal/SEB challenge and this protection was accompanied by suppression of systemic interleukin-2. However, rhG-CSF affected neither the proliferative responses of SAg-reactive T cells in vivo or in vitro nor their interleukin-2 production in vitro, implying that rhG-CSF may indirectly interfere with cytokine synthesis in T cells but not with T-cell-SAg binding itself. These results represent another beneficial effect of rhG-CSF as an antiinflammatory agent against T-cell-mediated toxicity triggered by SAg.

    UR - http://www.scopus.com/inward/record.url?scp=0029112465&partnerID=8YFLogxK

    UR - http://www.scopus.com/inward/citedby.url?scp=0029112465&partnerID=8YFLogxK

    M3 - Article

    C2 - 7543305

    AN - SCOPUS:0029112465

    VL - 86

    SP - 1420

    EP - 1427

    JO - Blood

    JF - Blood

    SN - 0006-4971

    IS - 4

    ER -