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PubMed2002

[Effects of macrophage colony-stimulating factor on production of estradiol and progesterone by human luteinized granulosa cells in vitro and detection of macrophage colony-stimulating factor receptor on human luteinized granulosa cells].

OBJECTIVE: To investigate the effects of macrophage colony-stimulating factor (M-CSF) on estradiol and progesterone production by human luteinized granulosa cells in vitro and to detect M-CSF receptor in human granulosa cells. METHODS: Human luteinized granulosa cells (LGC) were isolated from follicular fluid of superovulated infertile patients undergoing intracytoplasmatic sperm injection. Some of the LGC were used for detecting M-CSF receptor by immunocytochemical staining (ABC method). Most of them were cultured with HAM's F-10 medium plus various concentration of M-CSF (0, 10, 25, 50, 100, 250 ng/ml) in the presence or absence of follicle stimulating hormone (FSH). Media were collected at 72 hours after culture and estradiol (E(2)) and progesterone (P) in media were measured by enzyme immunoassays. RESULTS: About 80% of the LGC presented a positive M-CSF receptor staining with the immunochemical signal on cell membrane. After 72 hours culture of LGC, in absence of FSH, the baseline concentration of E(2) and P were (2,185 +/- 189) pmol/L, (3,157 +/- 401) nmol/L respectively; with the increasing dose of M-CSF from 10 to 100 ng/ml, the concentrations of E(2) increased from (2,789 +/- 365)pmol/L to (4,282 +/- 318) pmol/L, and those of P increased from (4,256 +/- 595) nmol/L to (7,789 +/- 828) nmol/L. In presence of FSH (75 IU/ml) the baseline concentrations of E(2) and P were (5,045 +/- 486) pmol/L and (8,667 +/- 923) nmol/L respectively; while the 10 - 100 ng/ml M-CSF was added the concentrations of E(2) and P were from (6,567 +/- 673) to (8,373 +/- 935) pmol/L and from (10,999 +/- 985) to (14,990 +/- 1,158) nmol/L respectively. Thus M-CSF caused a significant dose dependent increase of estradiol and progesterone production (P < 0.05), and M-CSF+ FSH further stimulated higher production of E(2) and P by LGC than M-CSF or FSH alone (P < 0.05). CONCLUSIONS: M-CSF receptor was expressed on membrane of human LGC. M-CSF enhances estradiol and progesterone production by LGC and FSH has an additional or synergetic effect with M-CSF.

Adult↗
PubMed1992

Interleukin-4 suppresses granulocyte colony-stimulating factor and granulocyte-macrophage colony-stimulating factor levels in stimulated human monocytes.

Granulocyte colony-stimulating factor (G-CSF) was quantitated in the supernatants of lipopolysaccharide (LPS)-treated human monocytes by ELISA. Unlike previous reports, the lymphokines, interleukin-4 (IL-4) and interferon-gamma (IFN-gamma), were unable to induce the synthesis of G-CSF. Both IL-4 (> or = 10 pM) and the glucocorticoid, dexamethasone (10(-7) M), inhibited G-CSF production in the LPS-treated monocytes; in contrast, IFN-gamma had a weak potentiating effect on the LPS action. Changes in antigen expression were manifested at the level of messenger RNA (mRNA). Granulocyte-macrophage (GM)-CSF in the LPS-treated monocyte supernatants was also quantitated by ELISA but its levels were somewhat lower than for G-CSF; IL-4, dexamethasone and IFN-gamma had similar effects on GM-CSF levels as on G-CSF levels. The suppression of CSF production in the stimulated monocytes by IL-4 and glucocorticoid extends the list of monocyte cytokines whose levels can be down-regulated by these agents and suggests another potential anti-inflammatory and immunosuppressive function for IL-4.

Cells, Cultured↗
PubMed1990

Acute and subacute hematologic effects of multi-colony stimulating factor in combination with granulocyte colony-stimulating factor in vivo.

Multi-colony stimulating factor (Multi-CSF, interleukin-3, IL-3) and granulocyte-CSF (G-CSF) administered concurrently as an intravenous (IV) injection induce a peripheral neutrophilia that is approximately additive in comparison with the neutrophilia induced by IL-3 and G-CSF individually. The bone marrow (BM) at 12 hours is depleted of mature neutrophils and shows a left-shifted myeloid hyperplasia, consistent with the neutrophil-releasing and myeloproliferative activities of both IL-3 and G-CSF individually. The BM at 24 hours shows a replenished reserve of mature neutrophils and a synergistic left-shifted myeloid hyperplasia as compared with IL-3 and G-CSF alone. Daily IV injections of IL-3 plus G-CSF for 1 week also induce an approximately additive daily peripheral neutrophilia. The BM after a week's administration of IL-3 plus G-CSF shows a generalized myeloid hyperplasia with a synergistic increase in mature neutrophils as compared with IL-3 or G-CSF alone. Daily injection of IL-3 plus G-CSF induced a significant decrease in erythroid, lymphoid, and eosinophilic marrow precursors, possibly owing to a myelophthisic effect of the myeloid hyperplasia and despite the fact that IL-3 alone induced a significant erythroid hyperplasia.

Animals↗
PubMed1982

Differences in the sensitivity of normal human peripheral blood and bone marrow granulocytic-macrophagic and eosinophilic colony forming cells (CFC) to a source of colony stimulating factor.

The relative sensitivity of normal human peripheral blood (PB) and bone marrow (BM) granulocytic-macrophagic and eosinophilic committed stem cells (CFC) to a source of colony stimulating factor (CSF) was evaluated. In this study, PB and BM cells depleted of mature granulocytes, monocytes (Mo), thymus dependent lymphocytes (T cells), and, in some studies, bone marrow derived lymphocytes (B cells) were cultured in soft agar medium. Human placental conditioned medium (HPCM) was used as a source of CSF. The time sequence evaluation of cultures of PB and BM cells in the presence of a constant amount of HPCM confirmed the results of earlier culture studies of unseparated PB and BM nucleated cells which showed that the proliferation of PB CFC is maximum at or after days 14 to 15 and that of BM CFC at days 7 to 8. Culture of a constant number of PB and BM cells with variable amounts of HPCM indicated that PB CFC require an exogenous source of CSF for proliferation whereas BM CFC proliferate to a modest degree in its absence. The rate of increase in the number of CFC proliferated with the addition of increasing amounts of HPCM is higher for BM than for PB. These data indicate that the BM CFC are more sensitive to a source of CSF than are the PB CFC. Also, the results of this study, along with those in the literature, support the concept that the PB and BM CFC comprise distinct populations, and, further, suggest that the PB CFC is more primitive than the day 7 BM CFC.

B-Lymphocytes↗
PubMed1993

Macrophage colony-stimulating factor and granulocyte-macrophage colony-stimulating factor stimulate the synthesis of plasminogen-activator inhibitors by human monocytes.

Macrophage colony-stimulating factor (M-CSF or CSF-1) and granulocyte-macrophage CSF (GM-CSF) have been shown to increase human monocyte urokinase-type plasminogen-activator (u-PA) activity with possible consequences for cell migration and tissue remodeling; because monocyte u-PA activity is likely to be controlled in part also by the PA inhibitors (PAIs) made by the cell, the effect of M-CSF and GM-CSF on human monocyte PAI-2 and PAI-1 synthesis was investigated. To this end, elutriation-purified human monocytes were treated in vitro with purified recombinant human M-CSF and GM-CSF, and PAI-2 and PAI-1 antigen and mRNA levels measured by specific enzyme-linked immunosorbent assays and Northern blot, respectively. Each CSF could enhance the protein and mRNA levels of PAI-2 and PAI-1 at similar concentrations for each product. This similar regulation of monocyte PAI expression in response to the CSFs contrasted with that found for the effects of lipopolysaccharide, transforming growth factor-beta and a glucocorticoid. Therefore, PAIs may be modulating the effects of the CSFs on monocyte u-PA activity at sites of inflammation and tissue remodeling.

Dose-Response Relationship, Drug↗
PubMed1997

Immunoreactive macrophage colony-stimulating factor is increased in atherosclerotic lesions of Watanabe heritable hyperlipidemic rabbits after recombinant human macrophage colony-stimulating factor therapy.

Infiltration of monocytes into arteries is an early event in the pathogenesis of atherosclerosis. This recruitment is interpreted as enhancing lesion development, but it could also be a host response limiting lipid accumulation. The ability of macrophages to limit cholesterol uptake, however, can be reduced by the impaired mobility and metabolic activity associated with foam cell development. As lesions enlarge, foam cells die and become the nidus for the necrotic core. Treatments to improve viability might improve foam cell function and promote regression. Macrophage colony-stimulating factor (M-CSF) is vital to monocyte/macrophage differentiation, proliferation, and activation. We found that foam cells of Watanabe heritable hyperlipidemic (WHHL) rabbits had faint staining for M-CSF. Treatment of rabbits with recombinant human M-CSF (rhM-CSF) increased M-CSF staining, which correlated with reduced cholesterol content of these foam cells.

Adipose Tissue↗
PubMed1994

Colony-stimulating factor-producing tumours: production of granulocyte colony-stimulating factor and interleukin-6 is secondary to interleukin-1 production.

We have reported that tumours producing colony-stimulating factor (CSF) also secrete interleukin-1 (IL-1) and IL-6. In the present study, we characterised the role played by IL-1 in CSF production. IL-1 receptor antagonist inhibited the production of granulocyte (G)-CSF and IL-6 by approximately 90% in CSF-producing human lung carcinoma cell lines. Similar results were obtained with hydrocortisone, which suppresses IL-1 gene expression. In contrast, 15 non-CSF-producing human lung carcinoma cell lines did not show detectable IL-1 production, although seven of them were induced to produce G-CSF and IL-6 by exogenous IL-1 alpha. Cell lines that responded to IL-1 alpha, including the CSF-producing lines, expressed receptors for IL-1 alpha. These results indicate that CSF-producing tumours can be characterised by their constitutive IL-1 production, IL-1 receptor expression and IL-1-dependent excess production of G-CSF and IL-6. Furthermore, transcription factor(s) may be involved in the abnormal IL-1 alpha production.

Blotting, Northern↗
PubMed1986

The effects in vivo of purified preparations of murine macrophage colony stimulating factor-1, recombinant murine granulocyte-macrophage colony stimulating factor and natural and recombinant murine interleukin 3 without and with pretreatment of mice with purified iron-saturated human lactoferrin.

The influence of purified natural colony stimulating factor-1 (CSF-1), purified recombinant granulocyte-macrophage (GM)-CSF, purified recombinant interleukin 3 (IL3) and natural IL3 were assessed in mice that were untreated or pretreated with purified iron-saturated human lactoferrin (LF) in order to first suppress myelopoiesis in the mice. S1/S1d mice responded to recombinant GM-CSF and recombinant IL3 in a manner similar to the response of their +/+ littermates. These 4 factors increased the cycling status of hematopoietic progenitors in vivo. The effects were more noticeable if myelopoiesis was first decreased by LF. The effects do not appear to be due to endotoxin contamination. It cannot be discerned from these studies whether the effects are direct ones on the progenitor cells or indirect ones mediated through growth-factor releasing accessory cells. It is possible that effects can be both direct and indirect.

Animals↗
PubMed2001

Dexamethasone increases the expression of membrane macrophage colony stimulating factor from retrovirally transduced tumor cells expressing macrophage colony stimulating factor.

Many different tumor cell types (breast, ovarian, glioma, liver and colon) were retrovirally transduced with the human macrophage colony stimulating factor (M-CSF) gene (either the membrane associated form [mM-CSF] or the secreted form [sM-CSF]). These cells were tested for their ability to display increased amounts of mM-CSF in response to dexamethasone. M-CSF-transfected tumor cells expressed additional mM-CSF in response to 18-72 h incubations with 3-15 microg/ml dexamethasone, while non-transfected parental cells were unaffected by this treatment. Increased mM-CSF protein expression on the M-CSF transduced cells was observed by flow cytometry and Western blotting using M-CSF specific antibodies. Northern blot analysis revealed an increase in the mM-CSF specific transcripts within the dexamethasone-treated mM-CSF transduced cells, but this was not seen within the non-transfected tumor cells that were treated with dexamethasone. ICAM-1 expression was unaffected by dexamethasone treatment, indicating that this response is mM-CSF specific. All trans-retinal and 1,25-dihydroxy vitamin D3 compounds that have been reported to induce M-CSF expression failed to increase mM-CSF. When dexamethasone-treated mM-CSF transfected clones were used as target cells for macrophage-mediated cytotoxicity assays, an increased killing with the dexamethasone-treated cells was seen. The macrophage-mediated cytotoxicity of these mM-CSF expressing tumor cells was blocked with excess recombinant M-CSF by saturating M-CSF receptors on the macrophage that is required for this form of tumor cell killing. This work suggests the possibility that dexamethasone may prove useful for vaccination purposes using mM-CSF retrovirally transfected tumor cells.

Animals↗
PubMed1998

The soluble granulocyte-macrophage colony-stimulating factor receptor's carboxyl-terminal domain mediates retention of the soluble receptor on the cell surface through interaction with the granulocyte-macrophage colony-stimulating factor receptor beta-subunit.

The hematopoietic cytokine granulocyte-macrophage colony-stimulating factor (GM-CSF) mediates its activity through binding to cell-surface receptors. The high-affinity GM-CSF receptor (GMR) consists of two transmembrane-anchored subunits: a ligand-specific, low-affinity subunit (GMRalpha); and a signal-transducing beta-subunit (GMRbeta). The human GMRalpha subunit also exists in a soluble isoform (SOLalpha) which antagonizes GM-CSF activity in vitro. Previous studies by us have shown that coexpression of SOLalpha and a mutated GMRbeta in BHK cells results in retention of SOLalpha on the cell surface and the formation of an intermediate affinity binding complex (Kd approximately 300 pM). This paper investigates the mechanism of the retention of SOLalpha on the cell surface. The data demonstrate that SOLalpha is anchored by a direct, ligand-independent interaction with GMRbeta which also occurs when SOLalpha is coexpressed with wild-type GMRbeta. However, SOLalpha and wild-type GMRbeta form a complex which binds GM-CSF with high affinity (Kd = 39 pM), indistinguishable from the binding characteristics of the TMalpha/GMRbeta complex. The experiments further reveal that the interaction between SOLalpha and GMRbeta is abrogated by removal of the unique 16 amino acid carboxyl-terminal domain of SOLalpha. Specific mutation of cysteine 323 in this carboxyl-domain to alanine also eliminates the cell-surface retention of SOLalpha identifying this residue as being necessary for the formation of the SOLalpha/GMRbeta complex.

Amino Acid Sequence↗
PubMed1997

Paclitaxel, ifosfamide and cisplatin with granulocyte colony-stimulating factor or recombinant human interleukin 3 and granulocyte colony-stimulating factor in ovarian cancer: a feasibility study.

The tolerability and efficacy of four courses of paclitaxel and ifosfamide plus cisplatin every 3 weeks was evaluated in patients with residual or refractory ovarian cancer. Additionally, supportive haematological effects of recombinant human interleukin 3 (rhIL-3) and recombinant human granulocyte colony-stimulating factor (G-CSF) were studied. Paclitaxel starting dose was 135 mg m(-2) (day 1), with ifosfamide dose 1.2 g m(-2) day(-1) (days 2-4) and cisplatin dose 30 mg m(-2) day(-1) (days 2-4). All 16 patients received 5.0 microg kg(-1) day(-1) G-CSF (days 7-16) and, in addition, eight patients were randomized to receive 10 microg kg(-1) day(-1) rhIL-3 (days 5-9). Paclitaxel and ifosfamide doses were reduced when grade IV haematological toxicity occurred. In the absence of grade IV haematological toxicity and normal recovery of haematopoiesis, paclitaxel dose was escalated. Toxicity was evaluable in 56 courses, with haematological effects in 52. Despite antiemetic treatment, nausea and vomiting (> or = grade I) occurred in 50 courses. Five patients had persisting peripheral neuropathy. Renal and liver function were not affected. Grade IV neutropenia occurred in 12 out of 52 courses, with neutropenic fever in two patients, both of whom died from fatal septicaemia. Grade IV thrombocytopenia without bleeding was observed in 15 courses. Grade IV haematological toxicity was associated with hepatic metastases and concurrent increases in alkaline phosphatase (P <0.001) and gamma-glutamyltransferase (P=0.007). No relation was found between haematological toxicity and pharmacokinetic parameters of paclitaxel. Patients treated with rhIL-3 showed a tendency to a faster platelet recovery (not affecting platelet nadir), and the cisplatin dose intensity was higher (P=0.025). Six of the nine evaluable patients had a tumour response. The overall median progression-free survival was 7 months and the overall mean survival was 13 months. In conclusion, this potentially interesting combination as second-line treatment showed a low tolerability with unexpected mortality, while rhIL-3 administration tended to induce a more rapid platelet recovery.

Adult↗
PubMed1987

Synergistic myelopoietic actions in vivo after administration to mice of combinations of purified natural murine colony-stimulating factor 1, recombinant murine interleukin 3, and recombinant murine granulocyte/macrophage colony-stimulating factor.

Combinations of low dosages of purified murine hematopoietic colony-stimulating factors (CSFs)--L-cell CSF type 1 (CSF-1), recombinant interleukin 3 (IL-3), and recombinant granulocyte/macrophage CSF (GM-CSF)--were compared with single CSFs for their influence on the cycling rates and numbers of bone marrow granulocyte/macrophage, erythroid, and multipotential progenitor cells in vivo in mice pretreated with human lactoferrin. Lactoferrin was used to enhance detection of the stimulating effects of exogenously administered CSFs. Concentrations of CSFs that were not active in vivo when given alone were active when administered together with other types of CSF. The concentrations of CSF-1, IL-3, and GM-CSF needed to increase progenitor cell cycling rates were reduced by factors of 40-200, 10-50, and 40- greater than 400, respectively; the concentrations needed to increase progenitor cell numbers were reduced by factors of 40-500 (CSF-1), 20-80 (IL-3), and greater than 40- greater than 200 (GM-CSF) when these forms of CSFs were administered in combination with low dosages of one of the other forms of CSFs. The results demonstrate that different CSFs can synergize when administered in vivo to increase the cycling rates and numbers of marrow hematopoietic progenitor cells. These findings may be of relevance physiologically to the regulation of myeloid blood cell production by CSFs.

Animals↗
PubMed1998

Adenovirus-mediated granulocyte-macrophage colony-stimulating factor improves lung pathology of pulmonary alveolar proteinosis in granulocyte-macrophage colony-stimulating factor-deficient mice.

Mutation of the granulocyte-macrophage colony-stimulating factor (GM-CSF) gene by homologous recombination causes progressive pulmonary alveolar proteinosis (PAP) in GM-CSF-deficient mice (GM-/-). The present study tested whether adenovirus-mediated expression of GM-CSF alters the progression of PAP in GM-/- mice. Adult mice were pretreated with an anti-T cell receptor (TCR) antibody to block T cell-mediated immune response, followed by intratracheal instillation of deltaE1-E3 replication-deficient adenovirus expressing mouse GM-CSF (Av1mGM). Mice were killed 1, 3, and 5 weeks after treatment to assess lungs for GM-CSF, surfactant protein B (SP-B), alveolar macrophage maturation, and type II cell proliferation. GM-CSF was detected in BAL fluid from GM-/- mice 1 week after Av1mGM treatment, and GM-CSF mRNA was detected by RT-PCR through 5 weeks. Five weeks after Av1mGM treatment, PAP was improved and SP-B decreased as assessed by ELISA and immunostaining. Increased numbers of alveolar macrophages stained with alpha-naphthyl acetate esterase (alpha-NAE) following treatment with Av1mGM. Local expression of GM-CSF with a recombinant adenovirus ameliorated PAP in the GM-/- mice in association with enhanced maturation of alveolar macrophages.

Adenoviridae↗
PubMed1997

The production of diaspora: Algerian emigration from colonialism to neo-colonialism (1840-1970).

"This paper is part of a larger project investigating the production and regulation of North African immigrants in the greater Paris automobile industry. Its aims are twofold. First, to reverse the emphasis placed on immigrants in the receiving countries and to (re-)explore the historical production of Algerian emigration into metropolitan industry, more specifically within the automobile industry....Second, in adopting an ¿articulation of modes of production' (AMOP) narrative as an alternative to other Eurocentric approaches, the first part of this paper emphasizes the contradictory layering of various modes which have produced an Algerian colonial diaspora. The latter half of the paper argues that the history of post-independence Algeria confirms that emigration was reinforced through a complex neocolonial relationship during a period of rapid acceleration of Algerian migration to France."

Africa↗
PubMed1977

Stimulation of human haemopoietic cells by colony stimulating factors: adherent cell dependent colony stimulating activity in human serum.

The number of granulocyte-macrophage clones formed in agar culture of bone marrow is dependent on levels of colony stimulating activity (CSA) a proposed in vivo haemopoietic regulator. A dose-response relationship for stimulation of human haemopoietic cells by CSA is demonstrated, which could be explained by thresholds of stimulation to cell division following a normal distribution. A simple method for the comparison of activities of test and control sources of CSA is presented. The apparent potentiating effect of the addition of two sources of CSA is explained by this dose-response relationhip. Haemopoietic cells from patients with chronic granulocytic or acute myeloid leukaemia showed the same dose-response relationship. CSA levels in normal human sera were greatly reduced by assay in the absence of adequate numbers of bone marrow "adherent cells" (cells adherent to nylon or plastic) or peripheral blood leucocytes, suggesting the presence of two kinds of CSA in human serum, one dependent on the presence of bone marrow adherent cells and one effective in their absence. Reduction of numbers of nonspecific esterase positive cells in the bone marrow sample correlated with reduction in the stimulating effect of serum. In all sera tested, adherent cell dependent CSA was the major component.

Cell Adhesion↗
PubMed1992

Polyethylene glycol (PEG) modification of granulocyte-macrophage colony stimulating factor (GM-CSF) enhances neutrophil priming activity but not colony stimulating activity.

PEG-modified proteins have numerous advantages over their unmodified counterparts (increased half life, reduced antigenicity, improved solubility), but almost without exception, they show a modest to marked reduction in biological or enzymatic activity. However, while investigating a new protocol for the preparation of PEG-proteins, we compared PEG-modified and unmodified GM-CSF with respect to their polymorphonuclear neutrophil granulocyte (PMN) priming activities. PEG-GM-CSF was unexpectedly more active than GM-CSF in its ability to prime neutrophils to respond to the synthetic peptide n-formyl-methionyl-leucyl-phenylalanine (FMLP) with an oxidative burst (assessed both by nitroblue tetrazolium reduction and ferricytochrome c reduction). These results were in contrast to the findings for colony stimulating activity and with GM-CSF induced thymidine uptake, where the biological activity was unchanged or reduced. The enhanced neutrophil priming activity of PEG-GM-CSF was confirmed using FPLC fractionated PEG-modified GM-CSF. This showed changes in the bioactivity profile consistent with both the shift in protein elution profile and enhanced activity of the PEG-modified material (reflected in the increased area under the bioactivity curve). We also excluded a neutrophil priming action for PEG-modified fetal calf serum proteins, carrier proteins and 'irrelevant' cytokine, erythropoietin. The dissociation of the two bioactivities was confirmed using individual FPLC fractions. These results suggest the presence of differences in either binding, receptor/ligand processing or signal transduction for neutrophils versus progenitors, that are differentially affected by PEG-modification of GM-CSF. The demonstration that PEG-modification can partially dissociate two biological activities suggests the feasibility of using PEG-modification to produce proteins with subtly altered spectra of biological activity and hence new ranges of clinical applications.

Cells, Cultured↗
PubMed2005

Granulocyte-colony stimulating factor primed bone marrow and granulocyte-colony stimulating factor mobilized peripheral blood stem cells are equivalent for engraftment: which to choose?

The first reported bone marrow transplant was published in 1939, although it was deemed unsuccessful. Between 1957 and 1965, numerous reports of bone marrow transplants, many of which were successful, were published for patients with irradiation injury, aplastic anemia, leukemia, lymphoma, and myeloma. Sources of marrow were autologous, isologous, and homologous (often unrelated, including cadaveric) donors. Bone marrow infusion was shown to be safe. It was also demonstrated that an aliquot of marrow, removed (harvested) from the ileum, had sufficient hematopoietic stem cells (SC) to repopulate the marrow and restore blood counts after myeloablation. For about 20 yr, bone marrow was the only source of hematopoietic stem cells (HSC) for transplantation. The first reported autologous peripheral blood HSC transplant was recorded in 1981 using chemotherapy 'mobilized' SC collected by leukapheresis. Mobilization is defined for these purposes to be any treatment that enhances the number of HSC in the blood such that the collection contains sufficient HSC to repopulate the marrow and restore blood counts after myeloablation. Since the early 1990s, SCT using blood-derived stem cells has become very popular and very common. The principal reason is that mobilized (whether by H growth factor or during recovery after chemotherapy) blood-derived stem cells engraft more rapidly than do marrow-derived stem cells. On the one hand, bone marrow was always harvested in the resting, unperturbed state (steady state). On the other hand, blood stem cells (BSC) were virtually always collected after mobilization, usually with granulocyte-colony stimulating factor (G-CSF). There is one report of collection of steady state BSC used for transplantation, and slow engraftment was documented. Bone marrow was never harvested after either chemotherapy or growth factor (priming). It is the mobilization (most often with G-CSF alone or after chemotherapy) of BSC that produces more rapid engraftment than for steady state marrow stem cells (MSC). This contribution shows the data that changes the old paradigm to a new paradigm which states bone MSC and BSC engraft identically if collected after the same pretreatment of the donor with growth factor.

Bone Marrow Transplantation↗
PubMed2006

Granulocyte-macrophage colony-stimulating factor inhalation therapy for patients with idiopathic pulmonary alveolar proteinosis: a pilot study; and long-term treatment with aerosolized granulocyte-macrophage colony-stimulating factor: a case report.

Idiopathic pulmonary alveolar proteinosis (IPAP) is considered to be caused by an autoantibody to the granulocyte-macrophage colony-stimulating factor (GM-CSF), which neutralizes GM-CSF and therefore impairs the differentiation of alveolar macrophages. The authors have previously characterized the BAL fluid and alveolar macrophages obtained from three IPAP patients who were successfully treated with aerosolized GM-CSF and demonstrated restoration of the cell number, expression of surface marker, and phagocytic ability of the alveolar macrophages as well as a decrease in the autoantibody levels in the BAL fluid. The condition recurred in one of the patients after 20 months. This patient underwent a second and third course of GM-CSF inhalation therapy with the same dose and schedule as the first one. Since the second therapeutic intervention did not succeed in producing any improvement in the symptoms and disease markers, the authors used a new nebulizer and a liquid preparation of the drug instead of the lyophilized preparation for the third therapeutic session and this restored the respiratory function considerably. A 6-month maintenance therapeutic regimen with a lower GM-CSF inhalation frequency brought about a further improvement in the disease markers. The results suggest that the efficacy of GM-CSF inhalation therapy might be related to the drug preparation mode, choice of nebulizer, and duration of treatment.

Aerosols↗