Abstract |
The macrocyclic lactone bryostatins, isolated from marine bryozoans, have been found to be strong inhibitors of e.g., the P 388 murine lymphocyte leukemia cell line and in vivo systems. Presently, bryostatin 1 is under preclinical development as a potential anticancer drug, although the bryostatins exhibit some of the same biological effects as the tumor promoting phorbol-12-myristate-13-acetate (PMA), especially activation of protein kinase C in certain cell types. In our experiments, we investigated the influence of bryostatin 1 on the synthesis of interleukin 2 ( IL2) and interferon-gamma (IFN-gamma) by ionophore A23187 or mitogen-induced human blood lymphocytes. These results were then compared with those achieved using the two tumor promotors PMA and teleocidin. Our data indicate that bryostatin 1 is comparable to these two other drugs in increasing production of the two lymphokines 10-100-fold. The IL2 and IFN-gamma production kinetics of cultures induced with either A23187/ bryostatin 1 or A23187/PMA were practically identical. The general pattern of peptides, however, released from bryostatin 1 coinduced cultures differed from that obtained when PMA was used.
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Authors | H Mohr, G R Pettit, A Plessing-Menze |
Journal | Immunobiology
(Immunobiology)
Vol. 175
Issue 5
Pg. 420-30
(Nov 1987)
ISSN: 0171-2985 [Print] Netherlands |
PMID | 3123367
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Research Support, U.S. Gov't, P.H.S.)
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Chemical References |
- Antineoplastic Agents
- Bryostatins
- Interleukin-2
- Lactones
- Lymphokines
- Macrolides
- Mitogens
- Calcimycin
- bryostatin 1
- Interferon-gamma
- Tetradecanoylphorbol Acetate
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Topics |
- Antineoplastic Agents
(pharmacology)
- Bryostatins
- Calcimycin
(pharmacology)
- Humans
- In Vitro Techniques
- Interferon-gamma
(biosynthesis)
- Interleukin-2
(biosynthesis)
- Kinetics
- Lactones
(pharmacology)
- Lymphocytes
(drug effects, immunology)
- Lymphokines
(biosynthesis)
- Macrolides
- Mitogens
(pharmacology)
- Tetradecanoylphorbol Acetate
(pharmacology)
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