Increase in histidine decarboxylase activity in tissues of mice bearing Colon-26 tumor cells

Takeuchi, Yoji; Nishibori, Masahiro; Uomoto, Masashi; Ishibashi, Hiromi; Nakaya, Naoki; Tanaka, Noriaki; Saeki, Kiyomi

doi:10.1007/s002109900037

Cited by 8 publications

(6 citation statements)

References 26 publications

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“…Therefore, it is speculated that inducible histamine may regulate the host immune response by modulating cytokine production in PBMCs. In the same context, it is noteworthy that the elevation of histidine decarboxylase activity was observed in the spleen and lung in tumorbearing animal models (29). It would be interesting to characterize the relationship between inducible histamine and the regulation of cytokine production.…”

Section: Discussionmentioning

confidence: 94%

“…In addition to the stable pool of histamine in mast cells and basophilic leukocytes, the presence of histamine with a different dynamic property, called inducible or nascent histamine, was suggested in the earlier works (24,25). Later, many groups reported the induction of histidine decarboxylase, a histamine-synthesizing enzyme, by LPS, cytokines, and lymphocyte mitogen in macrophages (26), T lymphocytes (27), and in many peripheral tissues (28,29). The synthesized histamine appeared not to enter the storage pool inside the cells, but rather was spontaneously released from the cells (30).…”

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confidence: 99%

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Histamine Is a Potent Inducer of IL-18 and IFN-γ in Human Peripheral Blood Mononuclear Cells

Kohka

Nishibori²,

Ishibashi³

et al. 2000

The Journal of Immunology

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Histamine (10−7 to 10−4 M) concentration-dependently stimulated the production of IL-18 and IFN-γ and inhibited the production of IL-2 and IL-10 in human PBMCs. Histamine in the same concentration range did not induce the production of IL-12 at all. The stimulatory or inhibitory effects of histamine on cytokine production were all antagonized by H2 receptor antagonists ranitidine and famotidine in a concentration-dependent manner, but not by H1 and H3 receptor antagonists. Selective H2 receptor agonists, 4-methylhistamine and dimaprit, mimicked the effects of histamine on five kinds of cytokine production. The EC50 values of histamine, 4-methylhistamine, and dimaprit for the production of IL-18 were 1.5, 1.0, and 3.8 μM, respectively. These findings indicated that histamine caused cytokine responses through the stimulation of H2 receptors. All effects of histamine on cytokine responses were also abolished by the presence of either anti-IL-18 Ab or IL-1β-converting enzyme/caspase-1 inhibitor, indicating that the histamine action is dependent on mature IL-18 secretion and that IL-18 production is located upstream of the cytokine cascade activated by histamine. The addition of recombinant human IL-18 to the culture concentration-dependently stimulated IL-12 and IFN-γ production and inhibited the IL-2 and IL-10 production. IFN-γ production induced by IL-18 was inhibited by anti-IL-12 Ab, showing the marked contrast of the effect of histamine. Thus histamine is a very important modulator of Th1 cytokine production in PBMCs and is quite unique in triggering IL-18-initiating cytokine cascade without inducing IL-12 production.

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Section: Discussionmentioning

confidence: 94%

mentioning

confidence: 99%

Histamine Is a Potent Inducer of IL-18 and IFN-γ in Human Peripheral Blood Mononuclear Cells

Kohka

Nishibori²,

Ishibashi³

et al. 2000

The Journal of Immunology

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“…LPS produced the induction of histidine decarboxylase, a histamine-synthesizing enzyme, in murine tissues (Endo, 1982), macrophages (Takamatsu et al, 1996), and T lymphocytes (Aoi et al, 1989). This induced histamine has been repeatedly suggested to have different kinetics from that in stored pools (Takeuchi et al, 1999) and may also have an immunomodulatory function. In addition to its inflammatory effects, histamine has immunomodulatory effects: regulation of cytotoxic T-cell activity (Khan et al, 1989), enhancement of natural killer (NK) cell activity (Hellstrand et al, 1994), and regulation of cytokine production in peripheral blood mononuclear cells (PBMCs) (Elenkov et al, 1998;Takahashi et al, 2002b).…”

Section: Figmentioning

confidence: 99%

Histamine Inhibits Lipopolysaccharide-Induced Tumor Necrosis Factor-α Production in an Intercellular Adhesion Molecule-1- and B7.1-Dependent Manner

Morichika¹,

Takahashi²,

Ishibashi³

et al. 2003

The Journal of Pharmacology and Experimental Therapeutics

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Lipopolysaccharide (LPS) is recognized as a key molecule in the pathogenesis of Gram negative sepsis and septic shock. In the present study, we demonstrate that LPS (1-1000 pg/ml) concentration dependently up-regulated the expression of intercellular adhesion molecule (ICAM)-1, B7.1, and B7.2 on human monocytes using fluorescence-activated cell sorting analysis, and that tumor necrosis factor (TNF)-␣ production induced by LPS in peripheral blood mononuclear cells (PBMCs) was inhibited by the addition of antibodies against these adhesion molecules, suggesting the dependence of TNF-␣ production on cell-cell interaction through these adhesion molecules. Moreover, we found that histamine (10 Ϫ7 -10 Ϫ4 M) concentration dependently inhibited the expression of ICAM-1 and B7.1, but not B7.2 on monocytes induced by LPS. Histamine also inhibited the responses of TNF-␣ production induced by LPS. The modulatory effects of histamine on ICAM-1 and B7.1 expression and TNF-␣ production were all concentration dependently antagonized by famotidine but not by d-chlorpheniramine and thioperamide, and were mimicked by selective H2-receptor agonists but not by H1-, H3-, and H4-receptor agonists, indicating the involvement of H2-receptors in the histamine action. Dibutyryl cAMP down-regulated ICAM-1 and B7.1 expression on monocytes stimulated by LPS, suggesting the mediation by the cyclic adenosine monophosphate-protein kinase A pathway of H2-receptor activation. These results as a whole indicated that histamine via H2-receptor inhibited the LPS-induced TNF-␣ production through the regulation of ICAM-1 and B7.1 expression, leading to the reduction of innate immune response stimulated by LPS.

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“…Mast cells of mice contain serotonin as well as histamine. Although we determined the histamine content and the number of mast cells in the liver, spleen and lung in the same tumour-bearing mouse model (Takeuchi et al 1999), we did not find any change in either of them. These findings suggest that the number of mast cells may be constant in this mouse model.…”

Section: Discussionmentioning

confidence: 69%

“…Yasumoto et al (1995) characterized the profile of cytokine production in this model. We also found specific tumour-bearing changes in monoamine dynamics in the brain (Uomoto et al 1998) and the induction of histidine decarboxylase in the peripheral tissues (Takeuchi et al 1999). Thus, this tumour-bearing animal model has been shown to be useful for the analysis of the changes in the neuro-immuno-endocrine (autacoid) environment in the body Yasumoto et al 1995;Uomoto et al 1998;Takeuchi et al 1999).…”

Section: Introductionmentioning

confidence: 84%

Changes in serotonin dynamics in the gastrointestinal tract of Colon-26 tumour-bearing mice: effects of cisplatin treatment

Nitta

Nishibori

Ishibashi

et al. 2001

Naunyn-Schmiedeberg's Archives of Pharmacology

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Severe nausea and vomiting are common side effects of anti-cancer chemotherapy. 5-HT3 receptor antagonists have been used for the treatment of these gastrointestinal symptoms. The purpose of this study was to examine whether specific changes in serotonin dynamics occurred in the gastrointestinal tract in mice in which Colon-26 adenocarcinoma cells were injected s.c., especially after treatment with cisplatin. The serotonin content of the small intestine of mice inoculated s.c. with Colon-26 adenocarcinoma increased significantly 2 weeks after the inoculation of the tumor cells; this was associated with an increase in tryptophan hydroxylase activity and the number of enterochromaffin cells as compared with control mice. Intravenous injection of cisplatin significantly reduced the serotonin content in the small intestine of Colon-26 tumour-bearing mice but not in control mice. The spontaneous release of serotonin from isolated intestine was not different between Colon-26 tumour-bearing and control mice; however, pretreatment of mice with cisplatin induced two fold increases in serotonin release from duodenum, jejunum and ileum in Colon-26 tumour-bearing mice but not in control mice. These results indicate that a region-specific increase in the number of enterochromaffin cells is observed in the intestine of Colon-26 tumour-bearing mice, associated with an increase in the serotonin content and tryptophan hydroxylase activity. Cisplatin treatment induced the release of serotonin from affected enterochromaffin cells in the gastrointestinal tract, which may be related to the occurrence of nausea in clinical use.

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Increase in histidine decarboxylase activity in tissues of mice bearing Colon-26 tumor cells

Cited by 8 publications

References 26 publications

Histamine Is a Potent Inducer of IL-18 and IFN-γ in Human Peripheral Blood Mononuclear Cells

Histamine Is a Potent Inducer of IL-18 and IFN-γ in Human Peripheral Blood Mononuclear Cells

Histamine Inhibits Lipopolysaccharide-Induced Tumor Necrosis Factor-α Production in an Intercellular Adhesion Molecule-1- and B7.1-Dependent Manner

Changes in serotonin dynamics in the gastrointestinal tract of Colon-26 tumour-bearing mice: effects of cisplatin treatment

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