Showing papers on "Macrophage proliferation published in 1985"

Induction of c-fos during myelomonocytic differentiation and macrophage proliferation.

Abstract: Previous studies have suggested a role for c-fos in cellular differentiation in fetal membranes1–3, haematopoietic cells4,5 and teratocarcinoma stem cells6. In other cell types, such as fibroblasts, c-fos expression is normally very low, but is rapidly induced by peptide growth factors, implicating c-fos in growth control mechanisms7–10. Here, we show that the TPA (12-O-tetradecanoylphorbol-13-acetate)-induced macrophage-like differentiation of HL60 human promyelocytic precursor cells11,12 is accompanied by the induction of both c-fos mRNA and protein within 15 min after treatment, suggesting a functional role for c-fos in this differentiation system. In quiescent terminally differentiated macrophages, expression of c-fos is inducible by the macrophage-specific growth factor colony-stimulating factor-1 (CSF-1)13. The kinetics of c-fos induction, however, are entirely different from those in growth factor-stimulated fibroblasts, supporting the view that the c-fos gene product may serve different functions in different cell types.

Endogenous regulation of macrophage proliferation and differentiation by E prostaglandins and interferon alpha/beta.

Abstract: Our results indicate that there are at least two levels of interaction involving M-CSF stimulation of committed stem cells and mature mononuclear cells. Mature cells residing in hematopoietic tissues produce both PGE and IFN alpha/beta upon recognition of CSF in their environment. In vitro, both of these mediators act to suppress CSF-induced colony formation in a negative feedback manner. However, additional evidence indicates that the endogenous IFN acts also to enhance functional maturation of the monocyte progeny. Cultures deprived of IFN during clonal expansion displayed severely depressed capacities to produce IL-1, to resist lytic HSV infection, and to phagocytose opsonized erythrocytes via Fc receptors. Thus, it appears that the result of M-CSF stimulation of a mature cell is the production of a differentiation signal (IFN alpha/beta), which in turn affects an immature cell of the same lineage that responds to the CSF-1 growth stimulus. Whether the Ia+ subpopulation of M-CSF responsive progenitor cells represents precursors for a separate cell lineage or a subclass of macrophages remains to be determined. Similarly, the regulation of these cells by PGE and IFN remains to be explored. However, within the parameters of our investigation, neither these cells nor their specific regulator, acidic isoferritin, were of consequence.

T cell involvement in production of tumor necrosis factor: reconstitution experiments with nude mice.

Abstract: In order to investigate the role of T cells in the production of tumor necrosis factor (TNF), a reconstitution experiment was performed with nude mice (Balb/c, nu/nu). The results obtained were as follows: 1) The cytotoxic activity of tumor necrosis serum (TNS) from Balb/c, nu/nu mice treated with Propionibacterium acnes-LPS was 1/22 of that from Balb/c, nu/+ mice. 2) TNF activity increased 14 times in reconstituted nude mice as compared to Balb/c, nu/nu mice. 3) The production of the cytotoxic activity per cell was investigated using T cell and macrophage fractions separated from the spleens of both Balb/c, nu/nu and Balb/c, nu/+ mice treated with P. acnes as a priming agent. Elicitation with LPS was done in vitro. Release of cytotoxic activity into the culture medium was observed in the macrophage fraction, but not in the T cell fraction. However, no significant species difference was found. 4) With P. acnes treatment, the population of macrophages in the spleens from Balb/c, nu/+ mice increased 25.5 times, whereas that from Balb/c, nu/nu mice only increased 6.8 times. The above results suggest that the mechanism of the incremental effect of T cells on TNF production was due to the promotion of macrophage proliferation during the priming period after injection of P. acnes.

Enhancement of colony‐stimulating‐factor–dependent clonal growth of murine macrophage progenitors and their phagocytic activity by retinoic acid

Abstract: The effect of retinoic acid (RA) on the colony-stimulating-factor-dependent clonal growth of myeloid progenitors was assessed in semisolid agar cultures of mouse bone marrow cells using L-cell-conditioned medium that gave rise to macrophage colonies, granulocyte colonies, and mixed macrophage-granulocyte colonies and clusters. RA was found to enhance the overall formation of myeloid colonies (about 50%) and clusters in 7-day cultures. The increase was due to an enhanced formation of macrophage colonies (70-250%) and clusters which reached a maximal value at about 3 microM RA. In 4-day cultures, the effect of RA on macrophage colony formation was biphasic with a maximal enhancement at 10 nM. RA suppressed granulocyte-colony formation in 4-day cultures. RA increased the phagocytic activity of bone-marrow-derived macrophages at all stages of differentiation and/or maturation in culture. The Fc-receptor-mediated erythrophagocytosis as well as the phagocytosis of heat-killed yeast cells (HK-yeast) and starch particles increased by RA treatment in a dose-dependent manner, reaching an increase of 100-200% of the activity expressed in the absence of RA. Peritoneal exudate macrophages likewise exhibited an increased phagocytic response to a variety of particles, at both physiological and pharmacological concentrations of RA. Expression of an RA-mediated increase in phagocytic activity required a prolonged incubation with RA (greater than 19 hr). The data suggest that RA may be of physiological relevance in the regulation of proliferation and function of hemopoietic cells. Therapeutic doses of RA may potentiate macrophage proliferation and function, elements that are crucial at all phases of the various defense mechanisms that the organism possesses.

Induction of macrophage growth by lipoprotein.

Abstract: Cell-free tumorous ascitic fluid stimulated growth of variously induced mouse peritoneal macrophages and resident macrophages in vitro. This induction of macrophage growth by the tumorous ascitic fluid was confirmed by autoradiography. The macrophage growth-stimulating activity was stable on heating at 100 degrees C, in contrast to that of macrophage growth factor (colony stimulating factor) previously reported. This heat-stable macrophage growth-stimulating activity was recovered in the lipoprotein fraction of tumorous ascitic fluid. The lipoprotein from heat-treated normal mouse serum also induced growth of macrophages. These results indicate that lipoprotein can induce macrophage proliferation, at least in vitro.