IL‐1α and TNFα act synergistically to stimulate production of myeloid colony‐stimulating factors by cultured human bone marrow stromal cells and cloned stromal cell strains

Caldwell, Jerry; Emerson, Stephen G.

doi:10.1002/jcp.1041590205

Cited by 23 publications

(15 citation statements)

References 60 publications

(35 reference statements)

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“…Despite stimulation with TNF-α, which also promotes the production of fibroblastic G-CSF, M-CSF, and GM-CSF [47,48], few [49][50][51], our findings do not confirm the same capacity for marrow stroma cells. This underlines the importance of endothelium in the induction of DC development and further implies that endothelial cells may produce a yet unidentified factor, which, in synergism with TNF-α, favors antigen-presenting cell differentiation from oligopotential myeloid progenitors.…”

Section: Development Of DC From Cd34contrasting

confidence: 67%

Tumor Necrosis Factor Alpha‐Stimulated Endothelium: An Inducer of Dendritic Cell Development from Hematopoietic Progenitors and Myeloid Leukemic Cells

et al. 2004

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Especially when exposed to inflammatory stimuli, endothelial cells (EC) have been shown to promote the maturation of monocytes into dendritic cells (DC) and the long-term proliferation of CD34 + cells by constitutive cytokine production and direct cellular contact. We therefore hypothesized that cytokine-stimulated EC would induce hematopoietic progenitor cells to develop into mature dendritic cells. To test this theory, human CD34 + cells derived from cord blood or leukapheresis products were cultured with a monolayer of either interleukin (IL)-1β β, IL-4, or tumor necrosis factor (TNF)-α α-stimulated human umbilical cord EC. The cells in suspension were analyzed weekly over a period of 6 weeks. IL-1β β supported cell expansion, whereas IL-4 had no effect on cell expansion or DC differentiation. Only TNF-α α-stimulated EC induced the development of mature, allostimulatory DC with a high expression of CD83, HLA-DR, CD1a, and costimulatory molecules like CD80 and CD86. Acute myeloid leukemia cells from the cell line Kasumi-1 also developed DC-like features when cocultured with TNF-α α-stimulated EC. Direct contact between endothelial and progenitor cells increased the number of developing DC. Cell cycle analysis and apoptosis studies demonstrated a reduced G 2 M fraction, an increased S fraction, and a decrease in TNF-α α-dependent apoptosis of DC developing in the presence of endothelial cells. As shown by electron and confocal microscopic studies, intimate interactions between EC and DC occurred, resulting in the internalization of the developing DC within the EC monolayer and a bidirectional exchange of proteins. We conclude that, via the action of TNF-α α, inflamed human endothelium can induce CD34 + and leukemic cells to differentiate into dendritic cells.

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Section: Development Of DC From Cd34contrasting

confidence: 67%

Tumor Necrosis Factor Alpha‐Stimulated Endothelium: An Inducer of Dendritic Cell Development from Hematopoietic Progenitors and Myeloid Leukemic Cells

et al. 2004

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“…These results are in accordance w ith published data. 11 In a variety of investigated systems, it has been shown that incubation with cAMP agonists causes a differential effect on the production of cytokines. While some cytokines, such as interleukin-6 and leukaemia inhibitory factor, are induced by increased intrace llular cAMP concentrations, the expression of other cytokines is inhibited.…”

Section: Discussionmentioning

confidence: 99%

cAMP analogues downregulate the expression of granulocyte macrophage colony‐stimulating factor (GM‐CSF) in human bone marrow stromal cells in vitro

Bug

Aman

Huber

et al. 1998

Mediators of Inflammation

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The stimulation of granulocyte macrophage-colony stimulating factor (GM-CSF) by interleukin-1 (IL-1) has been shown to be counteracted in different mesenchymal cell systems by cyclic adenosine monophosphate (cAMP) agonists. The aim of this study was the evaluation of different cAMP agonists on GM-CSF expression in human bone marrow stromal cells. Incubation of secondary haematopoietic progenitor cell deprived human stromal cell cultures with IL-1 or TNF-alpha induced GM-CSF protein expression in culture supernatants and GM-CSF-mRNA in adherent stromal cells. The coincubation with 8-bromo-cAMP (8BrcAMP), a water soluble cAMP analogue, inhibited this GM-CSF stimulation at the protein and the mRNA level. This effect was dose dependent with a maximal inhibition of about 65% occurring at a 8BrcAMP concentration of 0.75 mM. In addition to 8BrcAMP, other cAMP agonists such as dibutyryl-cAMP, forskolin, pertussis toxin, or prostaglandin E2 (PGE2) had the same inhibitory effect on GM-CSF stimulation by IL-1. Coincubation with the cyclooxygenase inhibitor indomethacin had no significant influence on GM-CSF expression in stromal cells. Our results provide evidence that the previously described inhibitory effect of cAMP agonist PGE2 on haematopoietic progenitor cells in vivo is, at least in part, mediated by modulating the expression of GM-CSF in bone marrow stromal cells.

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“…These data indicated low synthesis of GM-CSF by stromal cells from CDCL stimulated by seric factor(s), but high synthesis after the addition of IL-1b. Caldwell & Emerson (1994) also studied stroma from CDCL and found low levels of GM-CSF in the absence of IL-1b, contrasting with a high release rate after IL-1b stimulation.…”

Section: Discussionmentioning

confidence: 99%

Cytokines active on granulomonopoiesis: release and consumption by human marrow myeloid stromal cells

Sensebé¹,

Mortensen

Fixe³

et al. 1997

Br J Haematol

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Haemopoiesis is sustained and preferentially committed to granulomonopoiesis by myeloid stromal cells generated by colony‐derived cell lines (CDCL). Using ELISA and RIA, we studied, in the supernatant of cells from CDCL, the time course of interleukins 3 and 6 (IL‐3, IL‐6), stem cell factor (SCF), granulocyte‐macrophage, granulocyte and macrophage colony stimulating factors (GM‐CSF, G‐CSF and M‐CSF), macrophage‐inflammatory protein‐1α (MIP‐1α) and transforming growth factor β1 (TGF β1). IL‐6, GM‐CSF, M‐CSF and MIP‐1α were released into the supernatant after medium renewal and, except for M‐CSF, addition of IL‐1β. G‐CSF was detected only after addition of IL‐1β. SCF, contained in medium, first declined and then increased 24 h after medium renewal. Release of TGF β1 started 24 h after medium renewal and lasted until day 7. IL‐3, provided by horse serum, declined throughout the 7 d of observation. In conclusion, stromal cells from CDCL synthesized and released into the supernatant. IL‐6, GM‐CSF, G‐CSF, M‐CSF and MIP‐1α after stimulation by seric factor(s) and/or IL‐1β. TGF β1 was synthesized and released without any obvious extraneous stimuli. There is no definite argument for synthesis of soluble SCF and IL‐3. These data support a model where growth factors increase shortly after medium renewal, and negative regulators take over at a later time.

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IL‐1α and TNFα act synergistically to stimulate production of myeloid colony‐stimulating factors by cultured human bone marrow stromal cells and cloned stromal cell strains

Cited by 23 publications

References 60 publications

Tumor Necrosis Factor Alpha‐Stimulated Endothelium: An Inducer of Dendritic Cell Development from Hematopoietic Progenitors and Myeloid Leukemic Cells

Tumor Necrosis Factor Alpha‐Stimulated Endothelium: An Inducer of Dendritic Cell Development from Hematopoietic Progenitors and Myeloid Leukemic Cells

cAMP analogues downregulate the expression of granulocyte macrophage colony‐stimulating factor (GM‐CSF) in human bone marrow stromal cells in vitro

Cytokines active on granulomonopoiesis: release and consumption by human marrow myeloid stromal cells

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