Leukemia inhibitory factor production by rat mast cells

Marshall, Jean S.; Gauldie, Jack; Nielsen, L; Bienenstock, John

doi:10.1002/eji.1830230911

Cited by 31 publications

(11 citation statements)

References 21 publications

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“…Although we have identified LIF as a keratinocyte‐derived mast cell growth‐enhancing factor [8], LIF is also produced from activated mast cells [26]. Mast cells, thus, may regulate their proliferation by themselves through the secretion of LIF.…”

Section: Discussionmentioning

confidence: 99%

Leukemia inhibitory factor enhances mast cell growth in a mast cell/fibroblast co‐culture system through Stat3 signaling pathway of fibroblasts

et al. 2000

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Leukemia inhibitory factor (LIF) enhanced mast cell growth in a mast cell/3T3 fibroblast co-culture system, however the precise mechanisms have not been defined. Western blot analysis showed that bone marrow-derived mast cells failed to express both LIF receptor (LIFR) and gp130, whereas 3T3 fibroblasts expressed both LIFR and gp130. This result indicates that the activity of LIF for mast cell growth is mediated by 3T3 fibroblasts. Signal transducer and activator of transcription (Stat) 3-transfected 3T3 fibroblasts enhanced mast cell growth. In addition, dominant-negative Stat3-transfected fibroblasts blocked LIF-mediated mast cell growth in the co-culture system. In conclusion, LIF-induced mast cell growth in the co-culture system is mediated by an indirect pathway via 3T3 fibroblasts through activating Stat3 signaling pathway in 3T3 fibroblasts. ß

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Section: Discussionmentioning

confidence: 99%

Leukemia inhibitory factor enhances mast cell growth in a mast cell/fibroblast co‐culture system through Stat3 signaling pathway of fibroblasts

et al. 2000

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“…Other mast cell cytokine responses, including the production of IL-3 and GM-CSF, have been shown to be regulated at a posttranscriptional level (42), and our results may reflect a similar mechanism. In previous studies we have observed high levels of IL-6 mRNA expression after calcium ionophore (A23187) treatment under conditions that have not led to IL-6 expression at the protein level (7,43). Extensive previous studies have failed to demonstrate detectable levels of cell-associated IL-6 in rat PMC under any culture conditions, although recombinant IL-6 added to cell pellet preparations can be readily detected in "spiking" experiments (7).…”

Section: Discussionmentioning

confidence: 99%

Interleukin (IL)-10 inhibits long-term IL-6 production but not preformed mediator release from rat peritoneal mast cells.

Marshall¹,

Leal-Berumen²,

Nielsen³

et al. 1996

J. Clin. Invest.

150

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Mast cells have been implicated in a number of diseases involving chronic inflammation including asthma, rheumatoid arthritis, and inflammatory bowel diseases. They are a potent source of several cytokines, including IL-6 and TNF-␣ . Freshly isolated rat peritoneal mast cells will produce IL-6 in response to anti-IgE, LPS, PGE 1 , or PGE 2 ; however, the mechanisms by which such cytokine production is regulated are poorly understood. IL-10 is recognized as an important immunoregulatory cytokine with effects on T cell development and the production of inflammatory cytokines. IL-10 has previously been described to enhance mast cell development in the context of IL-3 and IL-4. In the current study, we have examined the ability of IL-10 to modulate rat peritoneal mast cell IL-6 and TNF-␣ production in response to a variety of stimuli. We have observed that recombinant murine IL-10 can inhibit the production of both IL-6 and TNF-␣ by mast cells without altering the degree of histamine release in response to anti-IgE. Concentrations of IL-10 as low as 0.2 ng/ml were sufficient to inhibit IL-6 production by LPS-or anti-IgE-activated cells significantly. IL-10 also inhibited PGE 1 -and PGE 2 -induced IL-6 production. The relative potency of IL-10 as an inhibitor of mast cell IL-6 production was highly dependent upon the stimulus used, with a 10-fold difference in the IC 50 for LPS-or anti-IgEactivated cells (0.21 ng/ml) and cells activated with a combination of LPS and PGE 2 (2.29 ng/ml). This suggests that prostanoids may limit the ability of IL-10 to modulate mast cell IL-6 production in the context of inflammation. These data have important implications for the regulation of mast cell IL-6 in inflammatory diseases involving prostanoid production and the effects of treatment with cyclooxygenase inhibitors. Our results also demonstrate a dual role for IL-10 on mast cells as a growth factor and inhibitor of cytokine production. ( J. Clin. Invest. 1996. 97:1122-1128.)

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“…In airway tissue, fibronectin is produced by epithelial and mesenchymal cells and is an important signal protein involved in the proliferation, migration and attachment of cells at sites of injury and inflammation (Rickard et al , 1993). LIF is also produced by mast cells isolated from the rat (Marshall et al , 1993). Given the proximity of mast cells to sensory nerves (Marshall & Waserman, 1995) and the epithelium (Lamb & Lumsden, 1982), the ability of mast cells to produce LIF may also be an important factor in the proliferative response following mucosal damage.…”

Section: Discussionmentioning

confidence: 99%

Localization of leukaemia inhibitory factor to airway epithelium and its amplification of contractile responses to tachykinins

Knight

McKay

Wiggs

et al. 1997

British J Pharmacology

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In neural tissue, leukaemia inhibitory factor (LIF) is an important trophic cytokine. In this investigation, we determined if LIF was present in human and guinea‐pig airways and examined the role of this cytokine in modulating airway responses to endogenous and exogenous tachykinins as well as muscarinic receptor and β‐adrenoceptor stimulation. The presence of LIF in both human and guinea‐pig airways was determined by immunohistochemistry. Guinea‐pig tracheal explants were incubated in CRML‐1066 media containing LIF (0.5, 5 or 50 ng ml−1) for periods of 3, 6, 24 and 48 h. Tracheal rings were then transferred to organ baths for measurement of isometric force in response to carbachol, capsaicin, the neurokinin1 (NK1) receptor agonist [Sar9,Met(O2)11]‐substance P (SP), the NK2 receptor agonist neurokinin A (NKA) and isoprenaline. LIF immunoreactivity was observed primarily in basally situated cells in the airway epithelium of both large and small airways. Less intense immunoreactivity was observed in vascular endothelium and glandular epithelium. Treatment with LIF (0.5 ng ml−1) for 3 and 6 h significantly increased contractile responses to capsaicin by 42% and 43%, respectively, compared to time controls, whereas higher concentrations of LIF (5 and 50 ng ml−1) enhanced capsaicin‐induced contractions only after 6 h. After 24 h, responses to capsaicin were not significantly different from 0 h control. Contractile responses to capsaicin following exposure to LIF at any concentration for 24 h were not significantly different from relative time control values. Responses to [Sar9,Met(O2)11]‐SP, carbachol and isoprenaline were not influenced by time in culture or by exposure to LIF for up to 48 h. Contractile responses induced by NKA were not influenced by 3 or 6 h exposure to LIF, but at 24 and 48 h the mean maximum contractile responses to NKA were significantly increased by 33% and 35%, respectively, compared to control. These results demonstrate that LIF is present in guinea‐pig and human airway epithelium, and modulates airway responses to tachykinins. In the acute setting LIF augments the capsaicin‐induced release of endogenous tachykinins, whilst in the longer term (>24 h), LIF increases airway smooth muscle responses to tachykinins via an NK2 receptor selective mechanism. We conclude that LIF may be an important effector molecule in the response of airways to injury or inflammation. British Journal of Pharmacology (1997) 120, 883–891; doi:

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Leukemia inhibitory factor production by rat mast cells

Cited by 31 publications

References 21 publications

Leukemia inhibitory factor enhances mast cell growth in a mast cell/fibroblast co‐culture system through Stat3 signaling pathway of fibroblasts

Leukemia inhibitory factor enhances mast cell growth in a mast cell/fibroblast co‐culture system through Stat3 signaling pathway of fibroblasts

Interleukin (IL)-10 inhibits long-term IL-6 production but not preformed mediator release from rat peritoneal mast cells.

Localization of leukaemia inhibitory factor to airway epithelium and its amplification of contractile responses to tachykinins

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