caa a22 4500 469074116 CHVBK 20180323132930.0 cr unu---uuuuu 170328e19920301xx s 000 0 eng 10.1007/BF01741857 doi (NATIONALLICENCE)springer-10.1007/BF01741857 Rat macrophage activation after treatment with the bleomycin group of antitumour antibiotics in vivo [Elektronische Daten] [Mark Micallef, Masuo Hosokawa, Yuji Togashi, Hiroshi Kobayashi] Summary: We have previously reported that bleomycin and its derivative peplomycin enhance the release of cytokines by rat spleen cells during mitogen-stimulated cell culture in vitro, but liblomycin, another derivative of bleomycin, decreases cytokine release to below untreated control levels. Cytokine release correlated well with the inhibition of subcutaneous tumour growth after treatment with equivalent doses of the three analogues. In contrast, ascites tumour growth is completely inhibited by liblomycin and appears to be at least partly macrophage-mediated because the antitumour effect can be significantly inhibited by carageenan. This study shows that bleomycin and its analogues activate rat peritoneal macrophages and increase interleukin-6 release, O2 − production, cell spreading, phagocytosis and random migration of macrophages, but only bleomycin enhances peritoneal macrophage invasion into a monolayer of rat lung endothelial cells in vitro. This study also shows that although liblomycin decreases spleen cell cytokine production and is less effective than bleomycin against subcutaneous tumour, as we have previously reported, the antitumour drug activates peritoneal macrophages and, compared to bleomycin, has a remarkable therapeutic effect on rat ascites tumour. Springer-Verlag, 1992 Bleomycin group nationallicence Macrophage activation nationallicence Macrophage infiltration nationallicence Ascites tumour nationallicence Micallef Mark Laboratory of Pathology, Cancer Institute, Hokkaido University School of Medicine, Kita-15, Nishi-7, Kita-Ku, 060, Sapporo, Japan aut Hosokawa Masuo Laboratory of Pathology, Cancer Institute, Hokkaido University School of Medicine, Kita-15, Nishi-7, Kita-Ku, 060, Sapporo, Japan aut Togashi Yuji Laboratory of Pathology, Cancer Institute, Hokkaido University School of Medicine, Kita-15, Nishi-7, Kita-Ku, 060, Sapporo, Japan aut Kobayashi Hiroshi Laboratory of Pathology, Cancer Institute, Hokkaido University School of Medicine, Kita-15, Nishi-7, Kita-Ku, 060, Sapporo, Japan aut Cancer Immunology, Immunotherapy Springer-Verlag 35/2(1992-03-01), 106-112 0340-7004 35:2<106 1992 35 262 https://doi.org/10.1007/BF01741857 text/html Onlinezugriff via DOI 1 research-article jats NATIONALLICENCE 856 40 https://doi.org/10.1007/BF01741857 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Micallef Mark Laboratory of Pathology, Cancer Institute, Hokkaido University School of Medicine, Kita-15, Nishi-7, Kita-Ku, 060, Sapporo, Japan aut NATIONALLICENCE 700 1- Hosokawa Masuo Laboratory of Pathology, Cancer Institute, Hokkaido University School of Medicine, Kita-15, Nishi-7, Kita-Ku, 060, Sapporo, Japan aut NATIONALLICENCE 700 1- Togashi Yuji Laboratory of Pathology, Cancer Institute, Hokkaido University School of Medicine, Kita-15, Nishi-7, Kita-Ku, 060, Sapporo, Japan aut NATIONALLICENCE 700 1- Kobayashi Hiroshi Laboratory of Pathology, Cancer Institute, Hokkaido University School of Medicine, Kita-15, Nishi-7, Kita-Ku, 060, Sapporo, Japan aut NATIONALLICENCE 773 0- Cancer Immunology, Immunotherapy Springer-Verlag 35/2(1992-03-01), 106-112 0340-7004 35:2<106 1992 35 262 Metadata rights reserved Springer special CC-BY-NC licence nationallicence BK010053 XK010053 XK010000 NATIONALLICENCE NATIONALLICENCE NL-springer