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At least 469 records · Page 26Linked to original sources
PubMed1993

Transcriptional activation of the macrophage colony-stimulating factor gene by IL-2 is associated with secretion of bioactive macrophage colony-stimulating factor protein by monocytes and involves activation of the transcription factor NF-kappa B.

Human peripheral blood monocytes (Mo) constitutively display the beta-chain of the receptor for IL-2, whereas expression of the IL-2R alpha-chain is not constitutive but inducible with IL-2. Here we report that binding of human IL-2 to its binding site leads to transcriptional activation of the macrophage CSF (M-CSF) gene in Mo resulting in accumulation of M-CSF mRNA and subsequent release of bioactive M-CSF protein as demonstrated by ELISA and inhibition of IL-2 induced release of an activity-stimulating growth of monocyte-type colonies by a neutralizing anti-M-CSF antibody. Transcriptional activation of the M-CSF gene by IL-2 is preceded by enhanced binding activity of the transcription factor NF-kappa B to its recognition sequence in the 5' regulatory enhancer region of the M-CSF gene. Moreover, using a heterologous promoter (herpes thymidine kinase) construct containing the NF-kappa B consensus sequence, it is shown that NF-kappa B binding by an IL-2-induced monocyte-derived nuclear protein confers reporter gene (human growth hormone) activity. Taken together, our findings indicate that IL-2 induces gene expression of M-CSF in human blood-derived Mo and provide evidence for involvement of NF-kappa B in transcriptional regulation of this gene.

Animals↗
PubMed1998

Malaria and colonialism in the German colonies New Guinea and the Cameroons. Research, control, thoughts of eradication.

German malaria research during the colonial period took place between medical and political interests. In the field of zoological and clinical research of malaria Germany was not a pioneer. Nevertheless, Robert Koch forced by impressive Italian results tried to participate in malaria research on the field of acquired malaria immunity and by optimizing the therapeutic doses of quinine in German New Guinea. In the German Cameroons, on the other hand, the fight against malaria was completely dominated by racial and political arguments. The paper tries to shed light on this dichotomy, which turned out to be not very productive.

Cameroon↗
PubMed1996

Effects of PIXY321, a granulocyte-macrophage colony-stimulating factor/interleukin 3 fusion protein, on human tumor colony-forming units taken directly from patients.

PIXY321, a granulocyte-macrophage colony-stimulating factor/interleukin 3 (GM-CSF/IL-3) genetically engineered hybrid, has shown greater biological activity in stimulating committed myeloid progenitors than either GM-CSF or IL-3 in vitro, in vivo, and in patients treated with high-dose chemotherapy. However, one concern is that PIXY321 may stimulate the proliferation of malignant cells which have functional GM-CSF or IL-3 receptors. Therefore, using a human tumor cloning assay, we have tested the effects of several concentrations of PIXY321 ranging from 0.1 to 100 ng/ml on tumor cells taken directly from 98 patients with solid tumors and Hodgkin's or non-Hodgkin's lymphomas. Of the 34 evaluable specimens, including 15 breast cancers, 5 ovarian cancers, 5 lung cancers, and 9 lymphomas, none showed stimulation of tumor growth. Interestingly, a significant inhibition of the tumor proliferation was seen in one breast cancer and in one large cell immunoblastic non-Hodgkin's lymphoma after continuous exposure of PIXY321. In conclusion, the use of PIXY321 to reduce myelosuppression after high-dose chemotherapy appears unlikely to result in stimulation of the growth of malignant cells in patients with lymphoma or cancers of the breast, lung, and ovary.

Breast Neoplasms↗
PubMed1995

Differential regulation of fyn-associated protein tyrosine kinase activity by macrophage colony-stimulating factor (M-CSF) and granulocyte-macrophage colony-stimulating factor (GM-CSF).

The proliferation and differentiation of macrophages are regulated by, among others, GM-CSF and M-CSF. Treatment of bone marrow nonadherent (NA) cells with M-CSF induced a greater percentage of NA cells into adherent cells, recognized as monocyte/macrophages, than did GM-CSF. The effect of GM-CSF and M-CSF on the activation of fyn kinase, a 59-kDa src family-related protein tyrosine kinase (PTK), was studied. Control cultures of bone marrow NA cells expressed only minimal levels of fyn kinase activity. Treatment of bone marrow NA cells with M-CSF, but not GM-CSF, for 12 to 24 h greatly enhanced the levels of fyn kinase activity. The effect of M-CSF on the activation of fyn kinase was further investigated using bipotential adherent bone marrow-derived macrophages (BMDMs) that coexpress receptors for both GM-CSF and M-CSF. BMDMs can be induced by either growth factor to undergo extensive proliferation in vitro. Compared to bone marrow NA cells, BMDMs displayed higher levels of basal fyn kinase activity, which were similarly elevated by M-CSF but not GM-CSF treatment. The role of fyn kinase in regulating cell adhesion was investigated by growing BMDMs in both tissue culture and Teflon flasks. The growth of BMDMs was anchorage independent; the majority of them continued to proliferate as cell suspension in Teflon flasks. Whereas the levels of fyn kinase activity in adherent BMDMs grown in tissue culture flasks increased steadily, those in BMDMs grown in Teflon flasks diminished. To study the role of fyn kinase in growth regulation, BMDMs were treated with c-fyn sense and antisense s-oligos. In the presence of c-fyn antisense s-oligos, the proliferative response of BMDMs to M-CSF but not GM-CSF was inhibited. In contrast, the proliferation of BMDM in response to either GM-CSF or M-CSF was not influenced by c-fyn sense s-oligos. Collectively, our data suggest that the activation of fyn kinase is closely associated with the acquisition of adherent capacity in maturing macrophages.

Animals↗
PubMed1988

Reliability of biotinylated DNA probes in colony hybridization: evaluation of an improved colony lysis method for detection of TEM-1 beta-lactamase.

Utilizing an improved method for colony hybridization developed by Haas & Fleming, biotin and 32P-labelled TEM-1 probes were compared for sensitivity and specificity in identifying the type of beta-lactamase made by over 100 clinical bacterial isolates. The new procedure was more reliable than a standard one, but still gave more than 20% false positive and false negative reactions.

Bacteria↗
PubMed2006

Farnesol restores wild-type colony morphology to 96% of Candida albicans colony morphology variants recovered following treatment with mutagens.

Candida albicans is a diploid fungus that undergoes a morphological transition between budding yeast, hyphal, and pseudohyphal forms. The morphological transition is strongly correlated with virulence and is regulated in part by quorum sensing. Candida albicans produces and secretes farnesol that regulates the yeast to mycelia morphological transition. Mutants that fail to synthesize or respond to farnesol could be locked in the filamentous mode. To test this hypothesis, a collection of C. albicans mutants were isolated that have altered colony morphologies indicative of the presence of hyphal cells under environmental conditions where C. albicans normally grows only as yeasts. All mutants were characterized for their ability to respond to farnesol. Of these, 95.9% fully or partially reverted to wild-type morphology on yeast malt (YM) agar plates supplemented with farnesol. All mutants that respond to farnesol regained their hyphal morphology when restreaked on YM plates without farnesol. The observation that farnesol remedial mutants are so common (95.9%) relative to mutants that fail to respond to farnesol (4.1%) suggests that farnesol activates and (or) induces a pathway that can override many of the morphogenesis defects in these mutants. Additionally, 9 mutants chosen at random were screened for farnesol production. Two mutants failed to produce detectable levels of farnesol.

Candida albicans↗
PubMed2004

Activation of human neutrophils by granulocyte colony-stimulating factor, granulocyte-macrophage colony-stimulating factor, and tumor necrosis factor alpha: role of phosphatidylinositol 3-kinase.

Stimulation of human neutrophils with granulocyte colony-stimulating factor (G-CSF), granulocyte-macrophage CSF (GM-CSF), or tumor necrosis factor alpha (TNF) resulted in phosphorylation of Akt, the potency being GM-CSF > G-CSF = TNF, which was inhibited by wortmannin. The findings indicated that phosphatidylinositol 3-kinase (PI3K) is activated by these cytokines. The possible participation of PI3K in activation of neutrophil functions induced by these cytokines was explored with PI3K inhibitors (wortmannin and LY294002). Superoxide release and adherence induced by GM-CSF or TNF were inhibited by PI3K inhibitors. Actin reorganization and morphological changes induced by G-CSF or GM-CSF were also inhibited by wortmannin, whereas these responses induced by TNF were unaffected by wortmannin. These findings suggested that PI3K is differentially involved in cytokine-mediated activation of neutrophil functions depending on the cytokines used. The results also showed that activation of extracellular signal-regulated kinase, but not p38 mitogen-activated protein kinase, induced by these cytokines is partly mediated by PI3K activation.

Androstadienes↗
PubMed1975

[Autoradiographic study of a bacterial colony. Application to the effects of polymyxin on Pseudomonas aeruginosa colonies].

The autoradiograph of a colony of Ps. a. which has been transferred, during growth, on a medium added with polymyxin and tritiate leucin makes it possible to locate an upper zone with a high metabolic activity and a basal zone with no metabolic activity. The latter, which consists of lysed cells, acts probably as a selective filter against the drug.

Autoradiography↗
PubMed1990

Precursors (pre-CFCmulti) of multilineage hemopoietic colony-forming cells quantitated in vitro. Uniqueness of IL-1 requirement, partial separation from pluripotential colony-forming cells, and correlation with long term reconstituting cells in vivo.

Pluripotential colony-forming cells (CFCmulti) from mouse marrow can expand significantly in number during 4 days of suspension culture with IL-1 and IL-3. In this study, the cells ("pre-CFCmulti") which originate this response are characterized in terms of their frequency, progeny number, factor requirements, buoyant density, and extent of restoration following marrow transplantation. Parallel measurements of both CFCmulti and cells providing long term marrow reconstitution in vivo allowed direct comparisons to be made with pre-CFCmulti. The proliferative response of pre-CFCmulti was found to depend uniquely on the combination of IL-1 and IL-3, and neither of these regulators was replaceable by any of IL-4, IL-6, IL-7, GM-CSF, G-CSF, M-CSF or LIF. After separation on density gradients, pre-CFCmulti were recovered in fractions of lower density than most of the CFCmulti, but in the same fractions that contained most of the in vivo reconstituting cells. After irradiation and marrow transplantation, marrow CFCmulti were restored to near normal levels, while both pre-CFCmulti as well as reconstituting stem cells remained profoundly depressed. These results show pre-CFCmulti to be distinct from most CFCmulti and to represent the closest approach to quantitative detection of reconstituting stem cells so far achieved in vitro.

Animals↗
PubMed1990

Monokine modulation of human astroglial cell production of granulocyte colony-stimulating factor and granulocyte-macrophage colony-stimulating factor. I. Effects of IL-1 alpha and IL-beta.

Granulocyte (G)-CSF and granulocyte-macrophage (GM)-CSF enhance phagocyte survival and function and are produced by fibroblasts and endothelial cells after induction by inflammatory mediators such as IL-1. Our ability to detect G-CSF and GM-CSF activity in the conditioned medium of the human astroglial tumor cell line, U87MG, and molecularly clone the cDNA for G-CSF from a U87MG cDNA library raised the possibility that astroglial cells are capable of G-CSF and GM-CSF production within the central nervous system; if so, the production of these CSF by astroglial cells may be inducible by IL-1. We examined the effects of IL-1 alpha and IL-1 beta on the production of G-CSF and GM-CSF by U87MG and U373MG, another astroglial tumor cell line that does not constitutively produce CSF. We demonstrate that both U87MG and U373MG can be induced to produce G-CSF and GM-CSF by exposure to IL-1 alpha and IL-1 beta. This response, measured by accumulation of increased CSF mRNA, is rapid, sensitive and due to the enhanced stability of CSF message following IL-1 exposure. The implications of these findings to the immunopathogenesis of central nervous system infections are discussed.

Astrocytoma↗
PubMed1993

Granulocyte-macrophage colony-stimulating factor, but not macrophage colony-stimulating factor, suppresses basal and lipopolysaccharide-stimulated complement factor production in human monocytes.

Monocyte/macrophage contribution of C biosynthesis is important, particularly during inflammation. Since granulocyte-macrophage CSF (GM-CSF) and macrophage-CSF (M-CSF) exert a variety of stimulatory effects on monocyte/macrophage functions in vitro, we studied their impact on the biosynthesis of the C components C3 and factor B by human monocytes in culture. GM-CSF at doses of 10 ng/ml and higher inhibited the basal C3 synthesis. This effect was most pronounced when the cytokine was added to freshly isolated monocytes. No effect was found on the basal production of factor B. Furthermore, GM-CSF abrogated the LPS-stimulated production of both C3 and factor B. These suppressive effects were neutralized by a polyclonal anti-GM-CSF antibody. Moreover, when anti-GM-CSF was added to unstimulated or LPS-stimulated cells, their C3 production increased. This indicates that both spontaneous and LPS-triggered release of monocyte-produced GM-CSF has an autocrine function in regulating monocyte C3 biosynthesis. GM-CSF also down-modulated the expression of CD14 at an early stage of cell culture. This might be the mechanism through which the LPS-effects are suppressed because CD14 has been shown to be a LPS receptor. Contrary to this, M-CSF at doses of 100 U/ml and higher stimulated the synthesis of C3, whereas the basal production of factor B and the LPS-stimulated production of C3 and factor B were unaffected. Granulocyte-CSF (G-CSF) did not influence monocyte C biosynthesis, and neither anti-M-CSF nor anti-G-CSF influenced the LPS-induced C3 production. The effects of GM-CSF and M-CSF on C biosynthesis may be important in regulating the availability of C components during an inflammatory response, and these observations may also have implications for the clinical use of CSF.

Antigens, CD↗
PubMed1998

MRL/lpr and MRL+/+ macrophage DNA synthesis in the absence and the presence of colony-stimulating factor-1 and granulocyte-macrophage colony-stimulating factor.

Macrophage accumulation and proliferation as well as altered macrophage properties have been observed in autoimmune MRL mice. To determine whether there might be innate differences in the proliferative responses, we examined the DNA synthesis responses of peritoneal macrophages and macrophages derived in vitro from bone marrow precursors (bone marrow-derived macrophages (BMM)). Murine peritoneal exudate macrophages normally require the addition of macrophage CSF (CSF-1) to enter cell cycle in vitro. In contrast, we have found that many thioglycollate-induced adherent peritoneal macrophages, but not resident peritoneal macrophages, from both MRL/lpr and MRL+/+ mice atypically underwent DNA synthesis even in the absence of added CSF-1. They also responded very well to granulocyte-macrophage CSF. These findings may help to explain the appearance of increased macrophage numbers in MRL lesions. In contrast to a previous report, it was found that MRL/lpr and MRL+/+ BMM did not have an enhanced response to CSF-1 and that modulation of CSF-1 receptor expression was not more rapid in MRL BMM. We also found no evidence for abnormal CSF-1 internalization and degradation or for the lpr mutation to have any enhanced effect on BMM survival in the absence of CSF-1. TNF-alpha lowered the DNA synthesis response to CSF-1 of MRL/lpr BMM rather than enhanced it, as has been reported. Our data suggest that the enhanced accumulation of macrophages in the MRL/lpr kidney cannot be explained by a proposed model of enhanced responsiveness of MRL/lpr BMM to CSF-1, including a contribution by TNF-alpha.

Animals↗
PubMed1995

Expression of granulocyte colony stimulating factor (G-CSF) and granulocyte/macrophage colony stimulating factor (GM-CSF) mRNA upon stimulation with phorbol ester.

Stimulated human peripheral blood mononuclear cells (MNC) have been shown to express both G-CSF and GM-CSF, Furthermore, G-CSF is expressed by monocytes but not lymphocytes, whereas GM-CSF is expressed largely by T lymphocytes and at low levels in monocytes/macrophages, Here we present the effect of TPA (120-O-tetradecanoyl phorbol-13-acetate) on G-CSF and GM-CSF expression in stimulated human MNCs and T lymphocytes. We observed that TPA (30nM) decreased G-CSF mRNA levels in MNCs, while ionomycin increased G-CSF in a dose-dependent manner. TPA and ionomycin individually increased GM-CSF mRNA levels in T-lymphocytes and MNCs. Further, GM-CSF was induced synergistically by TPA plus ionomycin, whereas this combination markedly decreased G-CSF mRNA levels in MNCs. These data suggest at least two signaling pathway by which G-CSF and GM-CSF and GM-CSF mRNA levels are modulated in a mixed population of monocytes and T lymphocytes, namely protein kinase C (PKC) and calcium. These signals seems to act synergistically in lymphocytes to increase GM-CSF, and not G-CSF mRNA levels specifically. It would also appear these signals act on MNCs in an opposing manner to decrease G-CSF mRNA levels, indicating that activation of PKC and the calcium signaling pathway lead to a cell-type specific modulation of individual cytokines and precise regulation of granulocyte production.

Adult↗
PubMed2001

Interleukin-10 contributes development of macrophage suppressor activities by macrophage colony-stimulating factor, but not by granulocyte-macrophage colony-stimulating factor.

Macrophages are known to possess suppressor activities in immune responses. To determine the effects of GM-CSF and M-CSF on the expression of macrophage suppressor activities, monocyte-derived macrophages cultured with GM-CSF (GM-Mphis) were compared with those cultured with M-CSF (M-Mphis) for antigen-specific proliferation and interferon-gamma (IFN-gamma) production by lymphocytes. Both GM-Mphis and M-Mphis equally suppressed lymphocyte proliferation, but only M-Mphis suppressed IFN-gamma production in response to purified protein derivative (PPD). M-Mphis, but not GM-Mphis, released IL-10 not only in the course of macrophage differentiation but also in response to PPD after maturation to macrophages. From the results that (i) exogenous IL-10 suppressed IFN-gamma production, but not proliferation of lymphocytes, and that (ii) neutralizing antibody to IL-10 reversed suppressor activities of M-Mphis on IFN-gamma production, but not lymphocyte proliferation, it appeared that IL-10 was the major factor responsible for suppression of IFN-gamma production. Thus, these results suggest that only M-CSF augments IL-10-dependent suppressor activity of macrophages on IFN-gamma production and that both GM-CSF and M-CSF induce IL-10-independent macrophage suppressor activity on lymphocyte proliferation.

Cells, Cultured↗
PubMed1996

Regulation of immunomodulatory functions by granulocyte-macrophage colony-stimulating factor and granulocyte colony-stimulating factor in vivo.

The present study was designed to investigate in vivo immunomodulatory properties of hematopoietic growth factors. The influence on the activation of cytokine synthesis and on the expression of surface antigens associated with cellular activation of G-CSF or GM-CSF was investigated in cancer patients receiving these factors. One single dose of growth factor was administered to patients with bladder cancer (G-CSF group) or small cell lung cancer (GM-CSF group) before chemotherapy. After cytoreductive chemotherapy patients received supportive therapy with G-CSF or GM-CSF. Peripheral blood mononuclear cells and plasma samples were obtained for flow cytometry, Northern blot analysis, and assessment of cytokine protein levels after single-dose as well as after continuous cytokine administration. Our results demonstrate differences in the induction of biological activities by GM-CSF and G-CSF in vivo which correlate well with in vitro findings. Among mature hematopoietic cells the effect of G-CSF is restricted to the granulocyte lineage. With GM-CSF moderate but unequivocal modulation of monocyte function was observed. On peripheral blood monocytes expression of MHC class-II molecules and CD44 was markedly stimulated. After one single dose of GM-CSF, plasma levels of sCD25 and IL-1RA were significantly induced (p < 0.0001, p = 0.032, respectively) and a trend to increased IL-8 levels was observed. The changes in plasma proteins were not correlated with shifts of mRNA expression for IL-8 and IL-1RA. T-cell activation was not observed with either cytokine. These results suggest that immunomodulatory features are differentially regulated by G-CSF and GM-CSF. The clinical relevance of a selective use of both hematopoietic growth factors in various disease settings remains to be determined.

Adjuvants, Immunologic↗