Recombinant human granulocyte-macrophage colony-stimulating factor stimulates in vitro mature human neutrophil and eosinophil function, surface receptor expression, and survival.

López, Angel F.; Williamson, Dominic J.; Gamble, Jennifer R.; Begley, C. Glenn; Harlan, John M.; Klebanoff, Seymour J.; Waltersdorph, A M; Wong, GG; Clark, SC; Vadas, MA

doi:10.1172/jci112705

Cited by 682 publications

(274 citation statements)

References 40 publications

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“…If IL-7 acted by mimicking GCSF or GM-CSF on myeloid progenitors, it failed to do so in mature neutrophils in vitro, which, despite expressing IL-7Ra, did not respond by increased survival, as do mature neutrophils in response to GCSF or GM-CSF. 28 The observation that IL-7 receptor signals can support myeloid development supports a stochastic model for myeloid differentiation, rather than an instructive model. Thus, in an instructive model, myeloid differentiation would require signals from a 'myeloid factor' like GCSF or GM-CSF, which our results show are not required and can be replaced by a 'lymphoid' factor, IL-7.…”

Section: Discussionmentioning

confidence: 99%

Retroviral transduction of IL-7Rα into IL-7Rα−/− bone marrow progenitors: correction of lymphoid deficiency and induction of neutrophilia

Jiang

Li²,

Aiello

et al. 2005

Gene Ther

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Defects in the gene for the IL-7 receptor (R) a chain are one cause of severe combined immunodeficiency disease (SCID) based on a strict requirement for IL-7 in T lymphoid development and survival. We tested the feasibility and potentially undesirable consequences of IL-7Ra gene transfer as a therapy for this genetic defect. The murine IL-7Ra gene was introduced into IL-7Ra À/À bone marrow progenitors using retrovirus and transplanted into Rag À/À recipient mice. Both ab and gd T cells were reconstituted in thymus and spleen showing proof of principle. B-cell development was also restored in some mice, but their numbers were much lower than in the T-cell compartment. Splenomegaly was observed due to an increase in neutrophils. We showed that hematopoeitic progenitors, after transfection with IL-7Ra, could respond to IL-7 in vitro by a striking production of neutrophils and other myeloid cells. These data indicate that although IL-7 is a critical lymphopoietin, ectopic expression of its receptor on multipotential progenitors can also induce production of myeloid cells, presumably through survival and proliferation signals that are not restricted to lymphoid cells. This supports the stochastic model of progenitor differentiation, in which cytokines give permissive and not instructive signals.

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Section: Discussionmentioning

confidence: 99%

Retroviral transduction of IL-7Rα into IL-7Rα−/− bone marrow progenitors: correction of lymphoid deficiency and induction of neutrophilia

Jiang

Li²,

Aiello

et al. 2005

Gene Ther

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“…It pro-longs the survival of eosinophils as well as neutrophils from the blood of normal volunteers in vitro by inhibiting apoptosis [18], promotes the release of monocytes, neutrophils and eosinophils from bone marrow [19] and enhances many of the biological functions of these cells [18]. However, ARDS is a disorder that specifically involves increases only in neutrophil numbers.…”

Section: Discussionmentioning

confidence: 99%

G-CSF and IL-8 but not GM-CSF correlate with severity of pulmonary neutrophilia in acute respiratory distress syndrome

Aggarwal¹,

Cs²,

Evans³

et al. 2000

Eur Respir J

174

124

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Activated neutrophils play a major role in the pathogenesis of acute respiratory distress syndrome (ARDS), and persistence of pulmonary neutrophilia is related to poor survival. Interleukin (IL)‐8 is implicated in recruiting neutrophils to the lungs but it has been postulated that granulocyte‐macrophage colony‐stimulating factor (GM‐CSF) and granulocyte colony‐stimulating factor (G‐CSF), which can promote the survival of neutrophils by delaying apoptosis, may prolong the inflammatory response. The aim of this study was to investigate the levels of GM‐CSF and G‐CSF in the lungs of patients with ARDS and determine their relationship relative to IL‐8 with levels of neutrophils and clinical outcome. The lungs of 31 patients with ARDS were sampled by means of bronchoalveolar lavage (BAL) and assays of the three cytokines were conducted via enzyme‐linked immunosorbent assay. GM‐CSF, G‐CSF and IL‐8 were all increased in the patients compared to healthy controls but concentrations of GM‐CSF were much lower than those of G‐CSF and IL‐8 (GM‐CSF

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“…IL-8 is chemotactic for neutrophils and some subsets of lymphocytes and is a direct activator of neutrophils (41,42), whereas IL-6 stimulates the proliferation and activation of T lymphocytes, and epithelial overexpression of IL-6 in transgenic mice leads to a marked lymphocytic infiltration of the airway (43,44). GM-CSF has been shown to enhance the survival and activation of both eosinophils and neutrophils (45)(46)(47).…”

Section: Discussionmentioning

confidence: 99%

Role of NF-κB in Cytokine Production Induced from Human Airway Epithelial Cells by Rhinovirus Infection

Kim

Sanders

Siekierski³

et al. 2000

The Journal of Immunology

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Infection of human epithelial cells with human rhinovirus (HRV)-16 induces rapid production of several proinflammatory cytokines, including IL-8, IL-6, and GM-CSF. We evaluated the role of NF-κB in HRV-16-induced IL-8 and IL-6 production by EMSA using oligonucleotides corresponding to the binding sites for NF-κB in the IL-6 and IL-8 gene promoters. Consistent with the rapid induction of mRNA for IL-8 and IL-6, maximal NF-κB binding to both oligonucleotides was detected at 30 min after infection. NF-κB complexes contained p65 and p50, but not c-Rel. The IL-8 oligonucleotide bound recombinant p50 with only about one-tenth the efficiency of the IL-6 oligonucleotide, even though epithelial cells produced more IL-8 protein than IL-6. Neither the potent glucocorticoid, budesonide (10−7 M), nor a NO donor inhibited NF-κB binding to either cytokine promoter or induction of mRNA for either IL-8 or IL-6. Sulfasalazine and calpain inhibitor I, inhibitors of NF-κB activation, blocked HRV-16-induced formation of NF-κB complexes with oligonucleotides from both cytokines, but did not inhibit mRNA induction for either cytokine. By contrast, sulfasalazine clearly inhibited HRV-16 induction of mRNA for GM-CSF in the same cells. Thus, HRV-16 induces epithelial expression of IL-8 and IL-6 by an NF-κB-independent pathway, whereas induction of GM-CSF is at least partially dependent upon NF-κB activation.

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Recombinant human granulocyte-macrophage colony-stimulating factor stimulates in vitro mature human neutrophil and eosinophil function, surface receptor expression, and survival.

Cited by 682 publications

References 40 publications

Retroviral transduction of IL-7Rα into IL-7Rα−/− bone marrow progenitors: correction of lymphoid deficiency and induction of neutrophilia

Retroviral transduction of IL-7Rα into IL-7Rα−/− bone marrow progenitors: correction of lymphoid deficiency and induction of neutrophilia

G-CSF and IL-8 but not GM-CSF correlate with severity of pulmonary neutrophilia in acute respiratory distress syndrome

Role of NF-κB in Cytokine Production Induced from Human Airway Epithelial Cells by Rhinovirus Infection

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