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T Tanimoto

Publications and source records attributed to T Tanimoto.

314 records · Page 18Linked to original sources
PubMedDate not supplied

Simultaneous exposure to interleukin-18 and interleukin-10 in vitro synergistically augments murine spleen natural killer cell activity.

Interleukin-18 (IL-18) enhances interferon gamma (IFNgamma) production and natural killer (NK) cell activity, and elicits protective antitumor effects in vivo. IL-18 and IL-12 synergistically augment IFNgamma production reportedly because IL-12 enhances IL-18 receptor (IL-18R) expression. We now show that IL-18 also synergizes with IL-10 to augment murine splenic NK activity against Yac-1 cells in a standard 4-h chromium-release assay, but IFNgamma production is only slightly enhanced. This pattern of NK activity was also observed with severe combined immunodeficient (SCID) mouse spleen cells indicating that the cytokines were not acting on T or B cells. The cytokines had no priming activity on the spleen cells and, when cells were left unstimulated for 24 h in culture, little NK activity was induced when IL-18 was added for the next 24 h. The reverse transcriptase/polymerase chain reaction revealed that IL-18 receptor (IL-18R) mRNA was expressed early during in vitro spleen cell culture but none was expressed after culture for 24 h regardless of the stimulus. Binding of 125I-labeled IL-18 revealed that exposure to IL-10 only slightly increased IL-18R expression. Expression of perforin mRNA was constitutive and was unaffected by the cytokines; however, Fas ligand (FasL) mRNA expression was strong in cultures with IL-18 alone or combined with IL-10. When Fas-expressing cells and their parental cells were used as targets, weak Fas-mediated cytolytic activity was observed after exposure to IL-18, and this was further enhanced by combination with IL-10. Finally, the augmentation of NK activity was abrogated by the inhibitor concanamycin A, indicating that the enhanced NK activity is perforin-dependent.

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PubMedDate not supplied

Nonsurgical treatment of posterior fossa epidural hematoma.

The recommended treatment for posterior fossa epidural hematoma has been prompt surgical evacuation. We report 2 patients who were treated conservatively. Both patients were younger than 10 years of age and developed subacute symptoms and signs. Serial computed tomography demonstrated complete resolution of the hematomas and no development of hydrocephalus during nonsurgical treatment. They recovered well without any neurologic deficits. In order to evaluate an indicative factor for nonsurgical treatment in young children with posterior fossa epidural hematoma, we review both of our patients and 36 well-documented patients from the literature, all of whom were younger than 10 years of age. The results demonstrate that the development of hydrocephalus is a critical factor in clinical progression. Nonsurgical management can be applied in these circumstances until spontaneous resolution of the hematoma unless early signs of medullary compression appear acutely after head trauma or serial computed tomography demonstrates the development of hydrocephalus followed by medullary compression.

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PubMedDate not supplied

Disturbance of myocardial energy liberation in experimental charcoal embolism of canine pulmonary artery.

Experimental charcoal embolism of the pulmonary artery was produced in dogs. Changes in hemodynamics, electrophysiology, and cardiac energy liberation were observed. The effects of histaminic and antihistaminic drugs on these changes were also studied. After two infusions of charcoal suspension, acute right ventricular overloading was recognized hemodynamically and electrophysiologically. Mitochondria isolated from both ventricles exhibited uncoupling of oxidative phosphorylation polarographically. These changes were enhanced with histamine injection and reduced with diphenhydramine injection. Histamine was seen to have some uncoupling effects on the heart mitochondria and a slight effect on cardiac dynamics. It is concluded that oxidative phosphorylation of the heart mitochondria was uncoupled in the acute stage of experimental pulmonary embolism, and that histamine might emphasize this change directly or indirectly or both, that is, directly affecting the myocardial cell metabolism, and indirectly aggravating myocardial hypoxia through pulmonary vasoconstrictive action.

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PubMedDate not supplied

Interleukin 18 enhances Fas ligand expression and induces apoptosis in Fas-expressing human myelomonocytic KG-1 cells.

Interleukin-18 (IL-18) induces apoptosis in human myelomonocytic KG-1 cells as determined by agarose gel electrophoresis, and flow cytometry after propidium iodide (PI) staining. Apoptosis was detected 20 hours from the start of culture at concentrations of 100 ng/ml of the cytokine. Although IL-18 induces the production of large amounts of interferon gamma (IFN-gamma) by KG-1 cells, conditioned media could not induce apoptosis of fresh cells. The protein expressions of p53 and Fas ligand by KG-1 cells, which constitutively express the Fas antigen (CD95), were found to increase after exposure to IL-18 for 20 hours. Both Fas ligand and its receptor were found to be functional by in vitro assays on Fas-expressing target cells and an agonist anti-Fas antibody, respectively. In conclusion, IL-18 enhances the expression of Fas ligand by Fas-expressing KG-1 cells and induces apoptosis in the cells through a mechanism probably involving the Fas pathway.

Apoptosis↗
PubMedDate not supplied

Augmentation of in vitro interleukin 10 production after in vivo administration of interleukin 18 is activated macrophage-dependent and is probably not involved in the antitumor effects of interleukin 18.

We have previously shown that interleukin (IL)-18 protects mice from intraperitoneal transplantation with syngeneic Meth A sarcoma, and in the process induces the production of large amounts of IL-10 from mitogen-stimulated treated mouse spleen cells, with a simultaneous augmentation of natural killer (NK) cell activity. Using in vivo and in vitro cell depletion methods, we now show that the cells producing IL-10 are neither NK cells nor macrophages (M phi), but that the IL-10 production is dependent on the presence of treated mouse M phi. Anti-IL-12 and anti-CD40L neutralizing antibodies could not inhibit the production of IL-10. Although IL-18-treated normal mouse enriched T cells stimulated with anti-CD3 and anti-CD28 antibodies failed to produce IL-10, the cytokine was also undetectable in culture supernatants of IL-18-treated nude mouse spleen cells, indicating that T cells were directly involved in the induced production of IL-10. Flow cytometry for intracellular IL-10 confirmed that CD8+ T cells and other, as yet unidentified spleen cell sub-sets were secreting IL-10, but only a small percentage of CD4+ cells produced IL-10. In vivo experiments using anti-IL-10 antibody indicated that IL-10 may not be directly involved in the antitumor effects of IL-18.

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