Efficient production of human tumour necrosis factor in Escherichia coli

Yamada, Masaaki; Furutani, Yasuji; Notake, Mitsue; Yamagishi, Jun‐ichi; Yamayoshi, Michiko; Fukui, Toshikazu; Nomura, Hideki; Komiya, M; Kuwashima, Junji; Nakano, K; Sohmura, Yasunobu; Nakamura, Shinichi

doi:10.1016/0168-1656(85)90015-x

Cited by 46 publications

(19 citation statements)

References 24 publications

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“…Lipopolysaccharide (E. coli; 055B5) was purchased from Difco Lab., Detroit, U.S.A.; reserpine (Apoplon) from Daiichi Seiyaku Co. Ltd., Tokyo, Japan and pargyline hydrochloride from Sigma Chemical Co., St. Louis, U.S.A. Recombinant human interleukin-la (IL-la) and recombinant human tumour necrosis factor a (TNFcc) were provided by Dainippon Pharmaceutical Co., Osaka, Japan, prepared according to Furutani et al, (1985) and Yamada et al (1985). Recombinant human IL-ifl was donated by the Ohtsuka Pharmaceutical Co., Tokushima, Japan and prepared according to Kikumoto et al (1987).…”

Section: Methodsmentioning

confidence: 99%

The effect of lipopolysaccharide, interleukin‐1 and tumour necrosis factor on the hepatic accumulation of 5‐hydroxytryptamine and platelets in the mouse

Endo

Nakamura

1992

British J Pharmacology

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Injection of lipopolysaccharide (LPS; 0.5–500 μg kg−1) into mice induced a dose‐dependent, slowly developing increase in hepatic content of 5‐hydroxytryptamine (5‐HT). This sustained increase could not be attributed to an LPS‐induced alteration of the pharmacokinetic handling of 5‐HT by stimulation of its uptake or inhibition of its degradation. Regional differences were apparent in the tissue content of histamine and 5‐HT between mast cell‐deficient (W/Wv) and normal (+/ +) mice. LPS administration (0.5 mg kg−1) gave comparable increases in the hepatic level of 5‐HT in mast cell‐deficient and normal mice. Reserpine pretreatment (1 mg kg−1) selectively reduced 5‐HT levels in the blood, spleen, liver, brain and lung of normal mice. Prior treatment with this agent also abolished the LPS (0.5 mg kg−1)‐induced hepatic accumulation of 5‐HT. Accumulation of 5‐HT in the liver by LPS (0.1 mg kg−1) was temporally associated with both a fall in the levels of circulating platelets, and a reduction in the concentration of 5‐HT in the blood. The LPS dose‐dependent (0.5–500 μg kg−1) increase in hepatic 5‐HT content was associated with a similar dose‐dependent reduction in the circulating levels of 5‐HT. Interleukin‐1, α and β (10 μg kg−1) and tumour necrosis factor α (TNFα) (1 mg kg−1) significantly enhanced the accumulation of 5‐HT within the liver. Administration of TNFα (10 μg kg−1) potentiated the increase in hepatic 5‐HT content seen with IL‐1β (10 μg kg−1). Electron microscopy revealed numerous platelets in the sinusoidal and perisinusoidal Disse spaces within the liver, in animals pretreated with LPS (0.1 mg kg−1). The platelets retained their intact structure and showed no evidence of degranulation. These data suggest that the LPS and cytokine‐induced mobilization of 5‐HT in the liver is associated with the hepatic translocation of platelets. This migration appears to be independent of platelet aggregation.

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Section: Methodsmentioning

confidence: 99%

The effect of lipopolysaccharide, interleukin‐1 and tumour necrosis factor on the hepatic accumulation of 5‐hydroxytryptamine and platelets in the mouse

Endo

Nakamura

1992

British J Pharmacology

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“…LPS of Escherichia coli 055B5, prepared by Boivin's method, was obtained from Difco Labs (Detroit, MI, U.S.A.). Recombinant human IL-lac and recombinant human TNF-xa, which were prepared according to Furutani et al (1985) and Yamada et al (1985), were provided by Dainippon Pharmaceutical (Osaka, Japan). Dichloromethylene diphosphonate was provided by Kissei Pharmaceutical (Matsumoto, Japan).…”

Section: Animals and Materialsmentioning

confidence: 99%

Effects of macrophage depletion on the induction of histidine decarboxylase by lipopolysaccharide, interleukin 1 and tumour necrosis factor

Endo

Nakamura

Nitta

et al. 1995

British J Pharmacology

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Our previous work has shown that injection into mice of lipopolysaccharide (LPS) and the cytokines interleukin 1 (IL‐1) and tumour necrosis factor (TNF) induces histidine decarboxylase (HDC), the enzyme forming histamine, in various tissues such as liver, lung, spleen and bone marrow, but not in the blood. The induction of HDC also occurs in nude mice and mast cell‐deficient mice. On the other hand, haematopoietic cytokines such as IL‐3, granulocyte colony‐stimulating factor (G‐CSF) and granulocyte – macrophage CSF (GM‐CSF) only induce HDC in the haematopoietic organs, i.e. bone marrow and spleen. In the present study, the effect of macrophage depletion on the induction of HDC was examined. On day 1 after a single intravenous injection of a macrophage depletor (liposomes encapsulating dichloromethylene diphosphonate, which is toxic when ingested into macrophages), macrophages were almost completely depleted in the liver and reduced by about 50% in the spleen and bone marrow, but not significantly affected in the lung. On day 3, the degrees of the depletion were similar to those of day 1. In the spleen, macrophages were depleted in the red pulp, and there was a structural destruction. In macrophage‐depleted mice, the induction of HDC by LPS, IL‐1α or TNF‐α was not impaired in the liver, and was potentiated in the lung and bone marrow. The induction of HDC was decreased only in the spleen at day 3. HDC was not induced by LPS in the spleen of the adult rat, which is correspondingly inactive in haematopoiesis. These results indicate that the major cells in which HDC activity is induced in response to LPS, IL‐1 and TNF are not circulating granulocytes, circulating monocytes, T cells derived from thymus, mast cells or phagocytic macrophages. Based on these results, we discuss the possibility that the major cells in which HDC was induced in non‐haematopoietic and haematopoietic organs were endothelial cells and haematopoietic precursor cells respectively.

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“…Because of its potential as an antineoplastic agent, considerable attention has been focused on this protein. Recently, human TNF has been purified to homogeneity (2), cloned, and expressed in X. coli (3)(4)(5)(6)(7)(8).…”

Section: Introductiqmentioning

confidence: 99%

Sendai virus induces high levels of tumor necrosis factor mRNA in human peripheral blood leukocytes

Berent¹,

Torczynski²,

Bollon³

1986

Nucl Acids Res

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ABSTRACSendai virus induces human peripheral blood leukocytes to produce high levels of tumor necrosis factor (TNF) mRNA. TNF mRNA can represent as much as 0.6% of the total mRNA. Kinetic studies indicate that the level of TNF mRNA peaks about 2 hours before that of IFN-a mRNA produced in the same system. Although the peak levels of TNF and IFN-a mRNA were similar, TNF in the culture supernatants was at a 200 fold lower level than IFN--. Cloning and sequence analysis of TNF cDNA isolated from peripheral blood leukocytes RNA showed that normal human cells in response to Sendai virus produce TNF identical to that previously isolated and cloned from tumor-derived cell lines. A bacterial expression system was used to produce the cloned TNF at a maximum level of 2 X 106 units per ml of culture.

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Efficient production of human tumour necrosis factor in Escherichia coli

Cited by 46 publications

References 24 publications

The effect of lipopolysaccharide, interleukin‐1 and tumour necrosis factor on the hepatic accumulation of 5‐hydroxytryptamine and platelets in the mouse

The effect of lipopolysaccharide, interleukin‐1 and tumour necrosis factor on the hepatic accumulation of 5‐hydroxytryptamine and platelets in the mouse

Effects of macrophage depletion on the induction of histidine decarboxylase by lipopolysaccharide, interleukin 1 and tumour necrosis factor

Sendai virus induces high levels of tumor necrosis factor mRNA in human peripheral blood leukocytes

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