Interleukin 1 stimulates fibroblasts to produce granulocyte-macrophage colony-stimulating activity and prostaglandin E2.

Zucali, James R.; Dinarello, Charles A.; Oblon, David J.; Gross, M.A.; Anderson, Lisa; Weiner, Roy S.

doi:10.1172/jci112512

Cited by 427 publications

(124 citation statements)

References 39 publications

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“…Accordingly, IL-1␣ increased their production and reduced this lag time and IL-1␣-prestimulated EC were more efficient in supporting this expansion than unstimulated cells. IL-1 is known to stimulate the secretion by EC of cytokines, some of them having functional importance in hematopoiesis such as IL-6, 60 colony-stimulating factors 61,62 or more recently LIF. 13,41 Although a direct effect of IL-1␣ on the progenitors cannot be ruled out, 63 our results suggest that it is mainly acting through the modulation of cytokine production by the stromal layer.…”

Section: Discussionmentioning

confidence: 99%

Endothelial cell support of hematopoiesis is differentially altered by IL-1 and glucocorticoids

et al. 1998

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Section: Discussionmentioning

confidence: 99%

Endothelial cell support of hematopoiesis is differentially altered by IL-1 and glucocorticoids

et al. 1998

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“…GM-CSF, which can be produced by T lymphocytes, monocytes, fibroblasts, and endothelial cells (13)(14)(15), has been recognized to stimulate functions of mature eosinophils (16), including antibody-dependent cytotoxicity (17,18), synthesis of leukotriene C4 in response to calcium ionophore stimulation (17), and cell-surface expression of antigens granulocyte function antigen 1 (GFA-1) and Mol (18 longed eosinophil survival in culture (18), and its presence was required to maintain the viability of eosinophils cultured with 3T3 fibroblasts (7). Utilizing the coculture system with 3T3 fibroblasts and GM-CSF, we have shown that eosinophils during in vitro culture can express HLA-DR. Because both fibroblasts and GM-CSF were needed to maintain eosinophil viability in culture as noted before (7), the specific roles of GM-CSF and fibroblasts in eliciting HLA-DR expression by eosinophils could not be determined.…”

Section: Methodsmentioning

confidence: 99%

Mature human eosinophils have the capacity to express HLA-DR.

Lucey

Nicholson‐Weller

Weller

1989

Proc. Natl. Acad. Sci. U.S.A.

146

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Human eosinophils are known to lose Ia antigen expression as they mature, and, accordingly, eosinophils obtained from the blood of five eosinophilic donors and three of four normal donors failed to display the major histocompatibility complex class II antigen HLA-DR, as determined by flow cytometry. However, when eosinophils from these nine donors were maintained in culture with recombinant human granulocyte-macrophage colony-stimulating factor and murine 3T3 fibroblasts, HLA-DR consistently developed on the eosinophils. By days 4-6 of culture, 24-97% ofeosinophils were HLA-DR+, and the eosinophils remained morphologically mature. In contrast, another class H antigen, HLA-DQ, was not detectable by flow cytometry on eosinophils from eight of nine donors. Cultured eosinophils were able to synthesize Culture of Eosinophils. Enriched eosinophils (1.5 x 106) were cultured in 3 ml of RPMI 1640 medium containing 10%6 (vol/vol) fetal calf serum and 150 units (=50 pM) of rhGM-CSF (expressed in yeast and purified to homogeneity; Genzyme) with an adherent monolayer of Swiss 3T3 fibroblasts (American Type Culture Collection) at 370C (5% C02/95% air) as described (7); 1.5 ml of culture medium was exchanged with fresh RPMI 1640/10% fetal calf serum/rhGM-CSF on days 2, 5, and 7. Nonadherent cells were collected on the indicated days; prior to flow cytometry, cell viability (>90%) was assessed with trypan blue and cell morphology was assessed by staining with phloxine-methylene blue and fast green-neutral red stains for eosinophils (8).Flow Cytometric Analyses. Flow cytometry (FACScan;Becton Dickinson) of 104 cells was performed after 5 x 10' eosinophils were stained with either 10 ,ul of fluorescein isothiocyanate-conjugated monoclonal antibodies for HLA-DR or CD5 (anti-Leu-1), both IgG K2a light chain (Becton Dickinson). Antigen expression was also assessed with fluorescein isothiocyanate-conjugated monoclonal antibodies (Becton Dickinson) for HLA-DQ, CD16 (anti-Leu-lla), and anti-Leu-M3. For comparison, HLA-DR expression was also evaluated on activated monocytes that had been isolated from peripheral blood, purified by adherence, and incubated for 24 hr with y-interferon (500 units, Sigma) as described (9).

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“…In addition, all of them have been initially identified as products produced by the classical immune-inflammatory cells (lymphocytes and monocytes) upon appropriate conditions of stimulation [45,46]. However, it is now clear that this group of cytokines can also be produced by other cell types, particularly structural cells, including fibroblasts, epithelial, endothelial and smooth muscle cells [47][48][49][50][51][52]. It is of interest to note that optimal conditions for the synthesis of these cytokines require IL-1 and/or TNF-α stimulation.…”

Section: Cytokinesmentioning

confidence: 99%

Immune-inflammatory functions of fibroblasts

Jordana¹,

Särnstrand²,

Sime³

et al. 1994

Eur Respir J

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Inflammation is a response that has evolved over millions of years to become an extremely complex process. This complexity reflects the host's need to deal effectively with a wide variety of potentially injurious agents, as well as the need to incorporate an adequate set of checks and balances. An inappropriately checked response, which occurs rarely, results in disease, either acute or chronic. However, in most instances, inflammation is a beneficial response, essential for survival. Inflammation comprises an extensive network of cellular interactions implemented by an overwhelming number of molecules. One category of signal includes soluble products, such as neuropeptide, lipid mediators, cytokines and growth factors, most of which can be produced by inflammatory/haemopoietic cells. However, resident structural cells can also produce many of these products and, on this basis only, fibroblasts, epithelial, endothelial and smooth muscle cells should be considered as active contributors to the regulation of the inflammatory response. Extracellular matrix (ECM) proteins comprise another category of signals. Whilst the most recognized activities of these proteins are those concerned with providing structural tissue integrity, it is clear that they also have powerful inductive effects. Indeed, ECM proteins can influence the shape, movement and state of activation of inflammatory cells in the tissue. Recent evidence indicates that these signals may also play substantial roles in homing of inflammatory cells to certain sites and in the handling of a number of cytokines and growth factors. In so far as fibroblasts are the main producers of ECM proteins, these new data establish an indirect but important role for fibroblasts in the regulation of the inflammatory response.

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Interleukin 1 stimulates fibroblasts to produce granulocyte-macrophage colony-stimulating activity and prostaglandin E2.

Cited by 427 publications

References 39 publications

Endothelial cell support of hematopoiesis is differentially altered by IL-1 and glucocorticoids

Endothelial cell support of hematopoiesis is differentially altered by IL-1 and glucocorticoids

Mature human eosinophils have the capacity to express HLA-DR.

Immune-inflammatory functions of fibroblasts

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