scholarly journals Production of colony-stimulating factor by leukemic leukocytes

Blood ◽  
1976 ◽  
Vol 47 (3) ◽  
pp. 381-388 ◽  
Author(s):  
JM Goldman ◽  
KH Th'ng ◽  
D Catovsky ◽  
DA Galton
Keyword(s):  
Peripheral Blood ◽  
Blood Cells ◽  
Peripheral Blood Cells ◽  
Colony Stimulating Factor ◽  
Monocytic Leukemia ◽  
Agar Culture ◽  
Normal Peripheral Blood ◽  
Stimulating Factor ◽  
Csf Production

The production of colony-stimulating factor (CSF) by the peripheral blood cells of untreated patients with acute myeloid leukemia (AML) was measured in the agar culture system using normal human bone marrow as the source of colony-forming units (CFUc). CSF production was found to be variable and was related to the morphologic subtype of AML--cells from patients with monocytic leukemia produced normal or large quantities of CSF, while (with one exception) those from patients with myeloblastic leukemia produced little or no CSF. There was a general relationship between CSF production and serum lysozyme levels. Attempts to demonstrate a consistent inhibitory effect exerted by leukemic peripheral blood cells on normal leukopoiesis in vitro were negative. Results instead suggested that the addition to the feeder layer of cells from patients with monocytic leukemia could raise CSF levels above those obtained with normal peripheral blood leukocytes alone, possibly by recruiting additional CFUc from normal marrow.

scholarly journals Production of colony-stimulating factor by leukemic leukocytes

Blood ◽  
1976 ◽  
Vol 47 (3) ◽  
pp. 381-388 ◽  
Author(s):  
JM Goldman ◽  
KH Th'ng ◽  
D Catovsky ◽  
DA Galton
Keyword(s):  
Peripheral Blood ◽  
Blood Cells ◽  
Peripheral Blood Cells ◽  
Colony Stimulating Factor ◽  
Monocytic Leukemia ◽  
Agar Culture ◽  
Normal Peripheral Blood ◽  
Stimulating Factor ◽  
Csf Production

Abstract The production of colony-stimulating factor (CSF) by the peripheral blood cells of untreated patients with acute myeloid leukemia (AML) was measured in the agar culture system using normal human bone marrow as the source of colony-forming units (CFUc). CSF production was found to be variable and was related to the morphologic subtype of AML--cells from patients with monocytic leukemia produced normal or large quantities of CSF, while (with one exception) those from patients with myeloblastic leukemia produced little or no CSF. There was a general relationship between CSF production and serum lysozyme levels. Attempts to demonstrate a consistent inhibitory effect exerted by leukemic peripheral blood cells on normal leukopoiesis in vitro were negative. Results instead suggested that the addition to the feeder layer of cells from patients with monocytic leukemia could raise CSF levels above those obtained with normal peripheral blood leukocytes alone, possibly by recruiting additional CFUc from normal marrow.

scholarly journals Dexamethasone and 1,25-dihydroxyvitamin D3, but not cyclosporine A, inhibit production of granulocyte-macrophage colony-stimulating factor in human fibroblasts

Blood ◽  
1991 ◽  
Vol 77 (9) ◽  
pp. 1912-1918 ◽  
Author(s):  
A Tobler ◽  
HP Marti ◽  
C Gimmi ◽  
AB Cachelin ◽  
S Saurer ◽  
...  
Keyword(s):  
Human Fibroblasts ◽  
Tnf Alpha ◽  
Colony Stimulating Factor ◽  
Dihydroxyvitamin D3 ◽  
Gm Csf ◽  
Macrophage Colony Stimulating Factor ◽  
Macrophage Colony ◽  
Stimulating Factor ◽  
Csf Production

Abstract Tumor necrosis factor alpha (TNF alpha) stimulates granulocyte- macrophage colony-stimulating factor (GM-CSF) production in human fibroblasts and other mesenchymal cells. However, relatively little is known about agents that downregulate cytokine production in these cells. In the present report we show that dexamethasone (Dexa), a synthetic glucocorticoid, markedly reduced GM-CSF production in TNF alpha-stimulated fibroblasts at both the protein and the RNA levels. CSF activity, GM-CSF protein, and RNA levels, determined by an in vitro colony-forming assay in normal human bone marrow cells, by an enzyme immunoassay, and by Northern blotting assay, were reduced to greater than 90% of control values by Dexa (1 mumol/L). Similarly, 1,25- dihydroxyvitamin D3 [1,25(OH)2D3], a hormone with possible physiologic immunoregulatory significance, reduced GM-CSF expression in a concentration- and time-dependent manner. However, this repression was less pronounced than that of Dexa, and in part due to a decreased proliferative activity. In contrast, cyclosporine A (CsA), another immunosuppressive agent, did not alter GM-CSF expression in TNF alpha- stimulated fibroblasts. Our in vitro studies suggest that by inhibiting GM-CSF production in fibroblasts, glucocorticoids and possibly 1,25(OH)2D3, but not CsA, may attenuate TNF alpha-mediated inflammatory processes and influence the regulation of hematopoiesis.

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