Tumoricidal response of liver macrophages isolated from rats bearing liver metastases of colon adenocarcinoma

C. Thomas*, A. M. Nijenhuis, B. Dontje, T. Daemen, G. L. Scherphof

*Corresponding author for this work

    Research output: Contribution to journalArticleAcademicpeer-review

    24 Citations (Scopus)

    Abstract

    Intraportal inoculation of CC531 adenocarcinoma cells into syngeneic rats causes an increase of liver macrophage cell number but not of major histocompatibility complex class II antigen expression. On day I after inoculation of 10(5) CC531 cells, a fixed number of isolated liver macrophages lysed significantly more target cells in vitro than did control cells, This effect was still present after 4 weeks. A 10-fold higher initial tumor dose significantly suppressed the macrophage response during the first 2 weeks. In contrast to tumoricidal activity induced by lipopolysaccharide in vitro, the tumoricidal response following in vivo challenge with tumor cells appeared not closely related to the production of reactive nitrogen intermediates, as in the latter case it was not abrogated in the presence of nitric oxide synthase inhibitor. Furthermore, the liver macrophage population appeared not fully activated after tumor inoculation as lipopolysaccharide further increased tumoricidal activity in vitro, The observed numerical and functional response of liver macrophages to intraportally inoculated tumor cells points at an important role of these cells in aspecific immune reactivity aimed at the reduction of local tumor growth, Results suggest that mechanistic differences exist between macrophage tumoricidal activity induced by tumor cells as compared with lipopolysaccharide.

    Original languageEnglish
    Pages (from-to)617-623
    Number of pages7
    JournalJournal of Leukocyte Biology
    Volume57
    Issue number4
    DOIs
    Publication statusPublished - Apr-1995

    Keywords

    • KUPFFER CELLS
    • LIVER MACROPHAGES
    • TUMOR CYTOTOXICITY
    • NITRIC OXIDE
    • MHC CLASS II
    • TUMOR-GROWTH
    • CANCER
    • CYTOTOXICITY
    • POPULATIONS
    • MECHANISMS
    • ALVEOLAR

    Cite this