## Abstract Spleen cells were collected from normal mice and cultured in a medium containing 20% calf serum. Addition of lipopolysaccharide (LPS) in the culture significantly increased the production of granulocyte‐macrophage colony‐stimulating factor (GM‐CSF), and a maximum induction was attained
A granulocyte-macrophage colony-stimulating factor (GM-CSF) produced by carrageenin-induced inflammatory cells of mice
✍ Scribed by M. Shikita; K. Tsuneoka; S. Hagiwara; S. Tsurufuji
- Publisher
- John Wiley and Sons
- Year
- 1981
- Tongue
- English
- Weight
- 801 KB
- Volume
- 109
- Category
- Article
- ISSN
- 0021-9541
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✦ Synopsis
Abstract
Seven days after subcutaneous injection of 2% carrageenin solution in mice, the induced inflammatory tissue was isolated and treated with 0.1% trypsin. When the dispersed cells were incubated in a nutrient medium containing 5‐‐20% calf serum, the cells grew adhering to the culture‐dish surface and colony‐stimulating factor (CSF) was accumulated in the medium gradually. Addition of lipopolysaccharide (Escherichia coli endotoxin) in the cell culture did not enhance the CSF production. It was shown by isoelectrofocusing that the majority of the produced CSF was an acidic molecule (pI = 3.8), while the treatment of this CSF with neuraminidase yielded a less acidic CSF species (pI = 5.1). Upon gel‐filtration chromatography in the presence of 6 M guanidine HCl, the CSF exhibited an apparent molecular weight of 42,000. On the other hand, polyacrylamide gel‐electrophoresis in the presence of 0.1% sodium dodecyl sulfate gave a molecular weight estimate of 65,000. Microscopic examination of the bone marrow cell culture showed that about one‐third of the colonies were granulocytic. Addition of prostaglandin E~1~(PGE~1~) in the bone marrow cell culture significantly inhibited the action of the CSF, while prostaglandin D~2~ was less inhibitory than PGE~1~. The result suggests that the cells isolated from the inflammatory tissue are capable of producing CSF, which may have a role for proliferation and maturation of the mononuclear phagocytes at the site of inflammation.
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