Granulocytopoiesis versus cytokine activities in peritoneal diffusion chamber cultures in the mouse.

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.

[Rapidly progressing glomerulonephritis]. / Hurtig progredierende glomerulonefritt.

20 patients with rapidly progressive glomerulonephritis were treated at the nephrological section, Medical Department A, Haukeland Hospital from 1973 to 1988. Nine patients had an idiopathic type of nephritis, while seven patients had this type of glomerulonephritis secondary to systemic lupus erythematosus, endocapillary glomerulonephritis, Henoch-Schönleins purpura or Wegener's granulomatosis. Four patients had antibodies to glomerular basement membrane. All renal biopsies showed extracapillary proliferation and tubular cell damage. All patients were given immunosuppressive treatment with corticosteroids and cytotoxic drugs. Nine patients who were admitted to the hospital from 1973 to 1978 were not treated with plasmapheresis, 11 patients from 1978-1988 were all treated with plasmapheresis. After one year of observation, six of the nine patients in the first group had died, while this applied to only two in the group treated with plasmapheresis. Early diagnosis and plasma exchange, in addition to immunosuppression, seems to be the best treatment for these patients.