Effects of in vivo administration of anti-IL-10 monoclonal antibody on the host defence mechanism against murine Salmonella infection

T. Arai, K. Hiromatsu, H. Nishimura, Y. Kimura, N. Kobayashi, H. Ishida, Y. Nimura, Yasunobu Yoshikai

    Research output: Contribution to journalArticle

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    Abstract

    Interleukin-10 (IL-10)is a cytokine that regulates various macrophage functions. To elucidate the involvement of endogenous IL-10 in the early stage of murine salmonellosis, we examined the effect of anti-IL-10 monoclonal antibody (mAb) administration on the host defence mechanism against Salmonella choleraesuis infection. The in vivo administration of anti-IL-10 mAb significantly enhanced host resistance at the early stage of Salmonella infection, as assessed by bacterial growth in the peritoneal cavity and the liver. Enhanced levels of monokine mRNA, including IL-1α, tumour necrosis factor-α (TNF-α) and IL-12, were observed from day 1 after infection in the peritoneal macrophages in anti-IL-10 mAb-treated mice compared with those in control mAb-treated mice. Mice treated with anti-IL-10 mAb exhibited significantly higher levels of interferon-γ (IFN-γ) in the peritoneal exudates and major histocompatibility complex (MHC) class II expression on the peritoneal macrophages on days 3 and 5 after infection. Notably, in vivo anti-IL-10 mAb brought about an increment of γδ T cells in the peritoneal cavity at the early phase of infection, which was correlated with the expression of endogenous heat-shock protein 60 (HSP60), which is implicated as a potential ligand for γδ T cells, in the infected macrophages. Our results suggest that the neutralization of endogenous IL-10 accelerates some macrophage functions and, consequently, the activation of immunocompetent cells, including γδ T cells, at the early stage of infection, resulting in an enhanced host defence against Salmonella infection.

    Original languageEnglish
    Pages (from-to)381-388
    Number of pages8
    JournalImmunology
    Volume85
    Issue number3
    Publication statusPublished - Jan 1 1995

    Fingerprint

    Salmonella Infections
    Interleukin-10
    Monoclonal Antibodies
    Macrophages
    Peritoneal Cavity
    Peritoneal Macrophages
    Infection
    T-Lymphocytes
    Monokines
    Chaperonin 60
    Exudates and Transudates
    Interleukin-12
    Major Histocompatibility Complex
    Interleukin-1
    Interferons
    Tumor Necrosis Factor-alpha
    Cytokines
    Ligands
    Messenger RNA
    Liver

    All Science Journal Classification (ASJC) codes

    • Immunology and Allergy
    • Immunology

    Cite this

    Arai, T., Hiromatsu, K., Nishimura, H., Kimura, Y., Kobayashi, N., Ishida, H., ... Yoshikai, Y. (1995). Effects of in vivo administration of anti-IL-10 monoclonal antibody on the host defence mechanism against murine Salmonella infection. Immunology, 85(3), 381-388.

    Effects of in vivo administration of anti-IL-10 monoclonal antibody on the host defence mechanism against murine Salmonella infection. / Arai, T.; Hiromatsu, K.; Nishimura, H.; Kimura, Y.; Kobayashi, N.; Ishida, H.; Nimura, Y.; Yoshikai, Yasunobu.

    In: Immunology, Vol. 85, No. 3, 01.01.1995, p. 381-388.

    Research output: Contribution to journalArticle

    Arai, T, Hiromatsu, K, Nishimura, H, Kimura, Y, Kobayashi, N, Ishida, H, Nimura, Y & Yoshikai, Y 1995, 'Effects of in vivo administration of anti-IL-10 monoclonal antibody on the host defence mechanism against murine Salmonella infection', Immunology, vol. 85, no. 3, pp. 381-388.
    Arai T, Hiromatsu K, Nishimura H, Kimura Y, Kobayashi N, Ishida H et al. Effects of in vivo administration of anti-IL-10 monoclonal antibody on the host defence mechanism against murine Salmonella infection. Immunology. 1995 Jan 1;85(3):381-388.
    Arai, T. ; Hiromatsu, K. ; Nishimura, H. ; Kimura, Y. ; Kobayashi, N. ; Ishida, H. ; Nimura, Y. ; Yoshikai, Yasunobu. / Effects of in vivo administration of anti-IL-10 monoclonal antibody on the host defence mechanism against murine Salmonella infection. In: Immunology. 1995 ; Vol. 85, No. 3. pp. 381-388.
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