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Y Fukutomi

Publications and source records attributed to Y Fukutomi.

33 records · Page 2Linked to original sources
PubMed1992

[Monokine production by mouse peritoneal macrophages after phagocytosis of mycobacteria].

It is well known that monokines, IL-1 (Interleukin-1) and TNF (Tumor Necrosis Factor), are produced by macrophages after stimulated with various agents. These cytokines are involved in various aspects of the inflammatory process and immunological response in addition to their original activities to proliferate T lymphocytes and causing tumor necrosis, respectively. Recently, there have been reported that IL-1 and TNF also play an important role in mycobacterial infections such as granuloma formation. In the present study, IL-1 and TNF productions were observed by mouse peritoneal exudate and resident macrophages after incubation with heat-killed M. lepraemurium and M. avium in vitro. The production was enhanced by phagocytosis of these mycobacteria in a dose dependent manner, and the time course of the production was maximum within 24 hr after phagocytosis of these mycobacteria. It was also shown of morphological changes and enhanced glucose consumption in media by these macrophages. Above results suggest that phagocytosis of mycobacteria by macrophages leads to monokine production, which would not only causes well known immunological reactions but also makes characteristic phenomena to be observed in mycobacterial infections.

Animals↗
PubMed1991

Tumor necrosis factor-alpha triggers antitoxoplasmal activity of IFN-gamma primed macrophages.

IFN-gamma is an important mediator of cellular resistance against microbial pathogens and tumor cells due in part to its potent capacity to activate macrophages for enhanced cytotoxicity. The present study demonstrates that TNF-alpha regulates the expression of enhanced antimicrobial activity by triggering IFN-gamma primed macrophages to kill or inhibit intracellular Toxoplasma gondii. Resident mouse macrophages stimulated with rIFN-gamma at levels up to 2500 U/ml failed to display enhanced antitoxoplasmal activity when cultured in vitro under low endotoxin conditions (less than 10 pg/ml), but were triggered by addition of small amounts of LPS (0.1 ng/ml). A similar requirement for LPS as a second signal necessary to trigger antitoxoplasmal activity was observed when IFN-gamma was administered to mice in vivo. The essential nature of this triggering step allowed us to explore the role of cytokines that act as endogenous regulators of macrophage activation. rTNF-alpha, although unable to confer antitoxoplasmal activity when used alone to treat macrophages, was capable of triggering IFN-gamma-primed macrophages cultured under low endotoxin conditions. The ability of TNF-alpha to trigger IFN-gamma-primed macrophages was blocked by rabbit anti-TNF-alpha polyclonal antisera but was not affected by polymyxin B indicating that TNF-alpha triggering was not due to contamination with LPS. Collectively, these findings demonstrate that TNF-alpha performs an important regulatory role in the expression of enhanced anti-microbial activity by IFN-gamma-primed macrophages.

Animals↗
PubMed1991

Reduced retinoid content in hepatocellular carcinoma with special reference to alcohol consumption.

Although alcohol is known to enhance hepatocarcinogenesis, the mechanism of this action remains to be explained. To test the hypothesis that ethanol depletes the liver of antitumor promoters such as retinoid, we measured the retinoid concentration in hepatocellular carcinoma tissues and noncancerous surrounding liver tissues in humans known to have a history of alcohol consumption. By high-performance liquid chromatography, the retinoid contents of 29 surgically resected hepatocellular carcinoma specimens and their noncancerous surrounding tissues were measured. Retinoid contents were decreased in both the cancerous and the surrounding noncancerous liver tissues of patients with a high intake of alcohol. The levels correlated inversely with the estimated cumulative lifetime ethanol consumption. The decrease in the retinoid content of hepatic parenchymal cells paralleled that in stellate cells. When compared with the surrounding liver tissues, the cancerous liver tissues were in the state of retinoid deficiency. In summary, alcohol abuse may help promote the hepatocarcinogenesis in man by depleting the liver of the antitumor promoter, retinoid.

Adult↗
PubMed1990

Inhibitory effects of acyclic retinoid (polyprenoic acid) and its hydroxy derivative on cell growth and on secretion of alpha-fetoprotein in human hepatoma-derived cell line (PLC/PRF/5).

Acyclic retinoid (polyprenoic acid) has a slightly different structure from retinoic acid. However, acyclic retinoid acts similarly to retinoic acid, because both bind to cellular retinoic acid-binding protein and cellular retinoid-binding protein. F-type, with the same strong binding affinity. We studied the effects of acyclic retinoid, the 7-hydroxy derivative of acyclic retinoid (7OH-acyclic retinoid) and retinoic acid on a human hepatoma-derived cell line PLC/PRF/5 (Alexander cells). Acyclic retinoid inhibited cell growth with an ID50 value of 14 microM, and reduced cell viability with an LD50 value of 86 microM. The ratios of LD50 value to ID50 value were 6.1 for acyclic retinoid, 2.4 for 7OH-acyclic retinoid and 1.4 for all-trans-retinoic acid. Taking this ratio as a parameter of relative cytotoxicity, we concluded that acyclic retinoid is the least toxic compound. Growth inhibition of cells by acyclic retinoid was associated with the incorporation of 3H-thymidine in the logarithmic phase. Acyclic retinoid reduced secretion of alpha-fetoprotein (AFP) and reciprocally increased secretion of albumin in the culture media, suggesting that acyclic retinoid influences gene expression of these proteins. Thus, acyclic retinoid, one of the less toxic retinoids, inhibits cell growth of human cancer cell line PLC/PRF/5 and appears to alter gene expression of AFP and albumin toward a "normal" direction.

Acrylates↗
PubMed1989

[A high risk group of hepatocellular carcinoma in man, with special reference to its clinical significance for the screening of early liver cancer. Gifu Study Group for Early Liver Cancer].

A high risk group of hepatocellular carcinoma (HCC) was statistically established using multiple regression analysis of 331 cases with liver cirrhosis (LC), in which 78 cases later developed HCC. Highly contributing factors to hepatocarcinogenesis were found to be positive HBsAg, age, drinking history, sex (male), history of blood transfusion, history of acute hepatitis (or jaundice) and elevated plasma levels of alpha-fetoprotein. A prospective study was initiated in April, 1985 employing another 122 LC patients to clinically evaluate the significance of the high risk group of HCC. 28 cases with small HCC (less than 3 cm in diameter) were newly found: 4 with chronic hepatitis and 24 with LC, among whom 22 developed from the high risk group (sensitivity 92%, specificity 44%). Three year survival rate of 28 cases thus found was 56%, and causes of death of 9 fatal patients were 4 cancer death, 4 hepatic failure and 1 gastrointestinal bleeding. In conclusion, the high risk group is valuable for the screening of early liver cancers, and treatments of hepatic failure as well as of HCC itself are important to improve the prognosis of HCC patients thus diagnosed.

Carcinoma, Hepatocellular↗
PubMed1988

Extrarenal Wilms' tumor in the adult patient. A case report and review of the world literature.

A case of an extrarenal Wilms' tumor arising in the retroperitoneal region of a 49-year-old male is reported. A review of the world literature indicates that the incidence of the tumor arising in the extrarenal region is extremely rare. A total of 14 cases have previously been reported, but the number of cases that occurred in adult patients is only 2. The clinical and pathologic features are briefly discussed.

Humans↗
PubMed1987

Augmentation of the antibody response by antigen-specific glycosylation-enhancing factor.

BDF1 mice were immunized with a protein antigen, such as ovalbumin (OA) or keyhole limpet hemocyanin (KLH), absorbed to aluminum hydroxide gel, and their spleen cells were stimulated by homologous antigen for the formation of glycosylation-enhancing factor (GEF). It was found that GEF obtained from OA-primed spleen cells had affinity for OA, whereas those derived from KLH-primed spleen cells had affinity for KLH. Nonspecific GEF, which was obtained by stimulation of normal spleen cells with pertussis toxin, failed to bind OA or KLH. Both antigen-specific GEF and nonspecific GEF are inactivated by phenylmethylsulfonyl fluoride, but not by N-alpha-p-tosyl-L-lysyl-chloromethyl ketone. Both factors can be partially purified by binding to p-aminobenzamidine agarose and elution with benzamidine. These findings suggest that not only non-specific GEF but also antigen-specific GEF are serine protease(s). The antigen-specific GEF consisted of two m.w. species, of 65 to 85 kilodaltons (Kd) and 40 to 55 Kd, whereas nonspecific GEF consisted of 50 to 70 Kd and 20 to 30 Kd molecules. The OA-specific GEF augmented the in vitro secondary indirect PFC response of DNP-OA-primed cells to the homologous antigen, but failed to affect the PFC response of DNP-KLH-primed cells to DNP-KLH. Similarly, KLH-specific GEF enhanced the response of DNP-KLH-primed cells but not the response of DNP-OA-primed cells. However, OA-specific GEF failed to replace the requirement for antigen-primed helper T cells. Antigen-specific GEF bound to alloantibodies reactive to the products of the I region of the major histocompatibility complex. The results collectively suggest that antigen-specific GEF is identical to antigen-specific augmenting factors described by other investigators.

Animals↗
PubMed1987

Formation of IgM-binding factors by murine thymocytes.

Normal mouse thymocytes activated with concanavalin A (Con A) released soluble factors which selectively inhibited rosette formation between human peripheral blood lymphocytes (PBL) and ox erythrocytes (Eo) sensitized with rabbit IgM antibodies. The factors were removed by absorption with mouse IgM-coupled Sepharose, and were recovered from the beads by elution at acid pH. They neither bound to mouse IgG-Sepharose nor inhibited rosette formation of PBL with Eo sensitized with rabbit IgG antibodies. Mouse IgM enhanced the formation of IgM-binding factors by Con A-activated thymocytes. Unstimulated normal mouse thymocytes also released IgM-binding factors upon incubation with mouse IgM. The molecular weights of IgM-binding factors were approximately 90-110 and 35-50 kDa as estimated by gel filtration. Each species of IgM-binding factors markedly suppressed the IgM-plaque-forming cell (PFC) response of sheep red blood cell-primed spleen cells and slightly suppressed the IgG PFC response.

Animals↗
PubMed1986

Dissociation of protective immunity against tuberculosis and tuberculin hypersensitivity at a level of lymphokines.

On the basis of present knowledge on the purification and the action mechanisms of macrophage regulating lymphokines, as summarized in Table VIII, tuberculosis immunity and tuberculin delayed type hypersensitivity may be dissociated at a level of responsible lymphokines. Table VIII. Dissociation of TB-IMM and DTH at a level of lymphokine 1. Purification of mediators resulted in separation of MIF/MAF and MCF 2. Anti-MIF antibody has no suppression of MCF reaction 3. Lipid metabolisms of macrophages stimulated with MIF/MAF and MCF are different 4. MIF/MAF suppresses MCF-reaction through monokines.

Animals↗
PubMed1982

Activation and augmentation of guinea pig macrophages with streptococcal preparation OK-432 and stimulated spleen cell products.

A mechanism of macrophage activation by a streptococcal preparation (OK-432) was studied. Peritoneal exudate macrophages from normal guinea pigs treated in vitro with OK-432 were activated, manifesting increased glucose consumption, increased spreading, and morphological alterations under scanning electron microscopy. Macrophages showed extensive spreading within 1 hr after OK-432 treatment; they then became rounded with characteristic ruffles in their surfaces after 6 hr of treatment. Highly purified macrophages were activated as effectively as a crude macrophage preparation, suggesting that the macrophage activation resulted from a direct interaction between macrophages and OK-432. However, when spleen cells were treated with OK-432, a factor(s) capable of activating macrophages was produced in the culture supernatant. Spleen macrophage-rich preparation was found to release the factor(s) upon stimulation with OK-432, but this did not occur with the lymphocyte-or granulocyte-rich preparations. These results indicate that OK-432 not only activates macrophages by direct interaction without lymphokine participation, but also augments the activation by affecting spleen cells, probably macrophages, in such a way as to produce monokines.

Animals↗