title: Granulocytopoiesis versus cytokine activities in peritoneal diffusion chamber cultures in the mouse.
abstract: Regulation of granulocyte formation was studied by correlating granulocytopoiesis in diffusion chambers with activities of putative regulatory cytokines in such chambers. The implantation procedure increased the levels in 1- and 2-d chambers of interleukin 6 (IL-6), G-CSF, TNF-alpha, and non-specific granulocyte/macrophage (G/M) colony-stimulating activities (CSA), assessed with bioassays and immunoassays. The activities subsided rapidly thereafter. They could be increased by vinblastine, cyclophosphamide, and a sterile inflammatory reaction (s.c. implanted copper rods; Cu-r). Anti-inflammatory indomethacin curtailed the IL-6, but raised the TNF-alpha, G-CSF, and CSA levels in Cu-r mice. Interferon inducer poly-I:C augmented G-CSF, but decreased TNF-alpha levels. Mouse blood cells cultured in chambers expanded their granulocyte/macrophage progenitor population rapidly during the first week of culture; this population being significantly larger on day 3 in perturbed than in unperturbed mice. A marked decline followed in the second week, significantly larger in mice given cytotoxic treatment than in controls. Peritoneal G-CSF and TNF-alpha may explain progenitor and granulocyte growth and development in diffusion chambers during the first week of culture. GM-CSF and IL-3 were apparently without any influence. None of the peritoneal cytokines assayed could explain the population decline during the second week, which was possibly caused by exhaustion of earlier progenitor cells, rather than by intra-chamber feedback mechanisms.
authors.affiliation: Department of Physiology, Institute of Basic Medical Sciences, University of Oslo, Norway.
authors.forename: X
authors.initials: X
authors.lastname: Wang
authors.forename: K B
authors.initials: KB
authors.lastname: Brekken
authors.forename: E M
authors.initials: EM
authors.lastname: Siebke
authors.forename: G
authors.initials: G
authors.lastname: Stokke
authors.forename: H K
authors.initials: HK
authors.lastname: Sørlid
authors.forename: H B
authors.initials: HB
authors.lastname: Benestad
mesh_terms: D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology; D000911:Antibodies, Monoclonal; D002478:Cells, Cultured; D003300:Copper; D003520:Cyclophosphamide / Q000494:pharmacology; D016207:Cytokines / Q000494:pharmacology*; D004058:Diffusion; D005260:Female; D016179:Granulocyte Colony-Stimulating Factor / Q000494:pharmacology; D006098:Granulocytes / Q000166:cytology*; D006410:Hematopoiesis; D006412:Hematopoietic Stem Cells / Q000166:cytology; D006801:Humans; D007213:Indomethacin / Q000494:pharmacology; D007249:Inflammation / Q000139:chemically induced / Q000473:pathology; D015850:Interleukin-6 / Q000494:pharmacology*; D008264:Macrophages / Q000166:cytology; D051379:Mice; D010537:Peritoneum; D011994:Recombinant Proteins / Q000494:pharmacology; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology; D014747:Vinblastine / Q000494:pharmacology
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D000911:Antibodies, Monoclonal; D016207:Cytokines; D015850:Interleukin-6; D011994:Recombinant Proteins; D014409:Tumor Necrosis Factor-alpha; D016179:Granulocyte Colony-Stimulating Factor; D014747:Vinblastine; D003300:Copper; D003520:Cyclophosphamide; D007213:Indomethacin