PMID- 2207323
OWN - NLM
STAT- MEDLINE
DCOM- 19901119
LR  - 20210216
IS  - 0006-4971 (Print)
IS  - 0006-4971 (Linking)
VI  - 76
IP  - 8
DP  - 1990 Oct 15
TI  - Coordinate secretion of interleukin-1 beta and granulocyte-macrophage 
      colony-stimulating factor by the blast cells of acute myeloblastic leukemia: role 
      of interleukin-1 as an endogenous inducer.
PG  - 1481-9
AB  - Acute myeloblastic leukemia (AML) blasts have been shown to produce a variety of 
      cytokines in culture such as interleukin-1 (IL-1), IL-6, granulocyte-, 
      macrophage-, and granulocyte-macrophage colony-stimulating factor (GM-CSF), and 
      tumor necrosis factor-alpha (TNF alpha). Using two sensitive and specific 
      enzyme-linked immunosorbent assays for IL-1 beta and GM-CSF, we document in the 
      present study that the production of the two cytokines by AML blasts in culture 
      is coordinated. First, we observe a striking correlation between the levels of 
      GM-CSF and IL-1 beta released by the cells. Thus, a high production of IL-1 beta 
      is always concordant with a high production of GM-CSF and, conversely, low 
      production of IL-1 beta is concordant with low levels of GM-CSF. Second, 
      neutralization of intrinsic IL-1 using antibodies that are specific for IL-1 
      alpha and -1 beta suppresses the release of GM-CSF by the cells. Third, 
      neutralization of the endogenous source of IL-1 also results in an abrogation of 
      GM-CSF mRNA. Fourth, the production of both IL-1 beta and GM-CSF is up-regulated 
      by exposing AML blasts to an exogenous source of IL-1, suggesting a positive 
      regulation of autocrine growth factor production. Taken together, our results 
      indicate that GM-CSF production by AML blasts is mediated by endogenously 
      produced IL-1. Both IL-1 beta and -1 alpha are produced by AML blasts, although 
      IL-1 beta appears to be more abundant. Spontaneous colony formation by AML blasts 
      is abrogated by the addition of neutralizing antibodies against IL-1 beta and 
      GM-CSF, whereas each antibody alone has little effect on blast proliferation. 
      Taken together, our results are consistent with the view that the production of 
      IL-1 beta by AML blasts supports autocrine growth in culture, through induction 
      of CSFs or other cytokines that stimulate blast proliferation.
FAU - Rodriguez-Cimadevilla, J C
AU  - Rodriguez-Cimadevilla JC
AD  - Clinical Research Institute of Montreal, Hotel-Dieu Hospital, Montreal, Quebec, 
      Canada.
FAU - Beauchemin, V
AU  - Beauchemin V
FAU - Villeneuve, L
AU  - Villeneuve L
FAU - Letendre, F
AU  - Letendre F
FAU - Shaw, A
AU  - Shaw A
FAU - Hoang, T
AU  - Hoang T
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Blood
JT  - Blood
JID - 7603509
RN  - 0 (Antibodies)
RN  - 0 (Interleukin-1)
RN  - 0 (RNA, Messenger)
RN  - 83869-56-1 (Granulocyte-Macrophage Colony-Stimulating Factor)
SB  - IM
MH  - Antibodies/pharmacology
MH  - Enzyme-Linked Immunosorbent Assay
MH  - Granulocyte-Macrophage Colony-Stimulating Factor/*blood/genetics/immunology
MH  - Humans
MH  - Interleukin-1/blood/pharmacology/*physiology
MH  - Leukemia, Myeloid, Acute/*blood/pathology
MH  - RNA, Messenger/metabolism
MH  - Tumor Cells, Cultured
EDAT- 1990/10/15 00:00
MHDA- 1990/10/15 00:01
CRDT- 1990/10/15 00:00
PHST- 1990/10/15 00:00 [pubmed]
PHST- 1990/10/15 00:01 [medline]
PHST- 1990/10/15 00:00 [entrez]
AID - S0006-4971(20)75217-1 [pii]
PST - ppublish
SO  - Blood. 1990 Oct 15;76(8):1481-9.