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Biomedical subjects

T Minagawa

Publications and source records attributed to T Minagawa.

At least 127 records · Page 7Linked to original sources
PubMed1985

Activation of natural resistance against lung metastasis of an adenocarcinoma in T-cell depressed spontaneously hypertensive rats by infection with Listeria monocytogenes.

We report here our study of the role of natural host defense mechanisms mediated by macrophages and natural killer (NK) cells in an experimental model of spontaneous pulmonary metastases of a mammary adenocarcinoma SST-2 in spontaneously hypertensive rats (SHR) with congenital T-cell depression. To activate macrophages and NK cells, Listeria monocytogenes (LM) was injected IV into SHR which had received a transplantation of SST-2. To assess the antimetastatic responses induced by LM, the number of lung nodules and the lung weight in SHR were evaluated 30 days after tumor inoculation. The growth of lung metastases, though not of primary tumors, was significantly reduced if 10(7) LM were injected IV into SHR 2, 10 and 20 days after the SC transplantation of 5 X 10(4) or 5 X 10(5) SST-2. An inhibitory effect of LM on pulmonary metastases was also observed in tumor-excised rats, in which the number of lung metastases and the lung weight were enhanced as compared with those in tumor-bearing rats which had not undergone surgery. Peritoneal resident cells which were harvested from rats injected with LM showed a significant augmentation of tumoricidal activity against SST-2 cells as measured by in vitro cytotoxicity. Similarly, the NK activity of spleen cells of SHR injected with LM increased significantly when compared with untreated SHR. These data suggest that the inhibition of metastatic growth, though not of primary tumor growth, was accomplished by the, possibly T-cell independent, activation of macrophages and NK cells.

Adenocarcinoma↗
PubMed1985

Purification of characterization of gene 8 product of bacteriophage T3.

The product of gene 8 (gp8) of T3 phage was purified from proheads, heads, and extract prepared from cells infected with a mutant defective in gene 10 (major head protein) (10- extract). gp8, when purified by hydrophobic column chromatography from proheads solubilized by guanidine hydrochloride, did not show any ordered structure. gp8 from heads ruptured by sucrose shock sedimented with a sedimentation coefficient of 20 S (20 S assembly). Electron micrography of 20 S assemblies showed ring structures displaying radial symmetry. When the gp8 in 20 S assemblies was concentrated, it formed two-dimensional crystals. gp8 in 20 S material was detected in 10- extract by sedimentation analysis. gp8 purified from 10- extract by anti-gp8 antibody column chromatography had an ordered structure identical to that of the 20 S assembly from heads. The effect of anti-gp8 serum on the activity of proheads and heads was examined by in vitro complementation. Anti-gp8 serum preabsorbed with 5- X 8- -extracted inactivated proheads and heads. Anti-gp8 serum preabsorbed with proheads inactivated heads but not proheads. Similarly, anti-gp8 serum preabsorbed with phage-inactivated proheads but not heads. From these results, it is concluded that gp8 in proheads and heads is accessible to antibodies and that different antigenic sites of gp8 are exposed in proheads and heads.

Antibodies↗
PubMed1985

Sequential production of alpha and beta interferons and gamma interferon in the circulation of Listeria monocytogenes-infected mice after stimulation with bacterial lipopolysaccharide.

Sequential production of interferon (IFN)-alpha/beta and IFN-gamma in the circulation of mice which had been previously infected with viable Listeria monocytogenes was induced by injection of lipopolysaccharide (LPS) derived from Salmonella typhimurium. IFN-alpha/beta production occurred 2 hr after injection of LPS, thereafter IFN-gamma appeared and the maximum titer was demonstrated at 6 hr. At that time, almost all of the IFN was IFN-gamma. IFN-gamma production in response to LPS was observed from the 5th through the 11th day after infection with Listeria, but it was not demonstrated in either mice infected with lower doses of viable Listeria or mice immunized with heat-killed bacteria. IFN-alpha/beta production was not drastically affected by treatment with hydrocortisone, cyclophosphamide, carrageenan, antithymocyte serum, or anti-asialo GM1 antibody, whereas IFN-gamma production was suppressed by administration of all those agents. Noteworthily, IFN-alpha/beta, but not IFN-gamma, was produced even 6 hr after stimulation with LPS in cyclophosphamide- or antithymocyte serum-treated mice. IFN-gamma induction by LPS was markedly suppressed in mice in which IFN-alpha/beta produced by Listeria infection itself had been depleted by treatment with anti-mouse IFN-alpha/beta antibody, but it was not inhibited in mice when IFN-alpha/beta induced not by Listeria infection but by LPS had been depleted by treatment with anti-mouse IFN-alpha/beta antibody.

Animals↗
PubMed1985

Natural killer cell numbers and function in peripheral lymphoid cells in Behcet's disease.

We have studied NK cell activity and numbers in the peripheral blood obtained from patients with Behcet's disease and from normal healthy controls. NK cell activity in the peripheral blood of patients in the clinically-active stage of Behcet's disease was significantly lower than that of patients in the inactive stage and normal controls. In contrast, it was observed that the actual number of NK cells was markedly increased in the peripheral blood of patients with active disease. The addition of alpha-interferon (INF-alpha) to these cells showed significant augmentation of NK cell activity. These results suggest that the patients with active Behcet's disease lack a factor which activates NK cells.

Adult↗
PubMed1985

Induction of alpha/beta interferon and gamma interferon in mice infected with Listeria monocytogenes during pregnancy.

Alpha/beta interferon (IFN-alpha/beta) was induced in the bloodstream of mice 48 h after intravenous infection with Listeria monocytogenes, whereas IFN-gamma was induced in the bloodstream 6 h after stimulation with specific antigen on day 5 of infection in virgin mice. In contrast, no IFN-alpha/beta or IFN-gamma was produced in the bloodstream of pregnant mice after L. monocytogenes infection. However, unusual acid-labile IFN-alpha/beta instead of IFN-gamma was produced in some of the pregnant mice in response to specific antigen. The bacterial growth in the organs of pregnant mice in the early stage of infection was normal, but resulted in the delay of T-cell-dependent elimination of bacteria from the organs of pregnant animals in the late stage, and numerous bacteria were detected in both the placenta and the fetus. The significance of the IFN system induced by L. monocytogenes infection in pregnant mice is discussed.

Animals↗
PubMed1984

The significance of alpha/beta interferons and gamma interferon produced in mice infected with Listeria monocytogenes.

Interferon (IFN)-alpha/beta was induced in the circulation of mice infected intravenously with Listeria monocytogenes 24 to 72 hr after infection, but was not induced by the administration of heat-killed Listeria, listerial cell wall fraction (LCWF), or listerial soluble fraction. Appearance of IFN-alpha/beta showed a pattern similar to that of the growth of bacteria in the spleen and the liver of mice. IFN-alpha/beta production was abrogated by pretreatment of mice with anti-asialo GM1 antibody, antithymocyte serum, or hydrocortisone, but not with cyclophosphamide or carrageenan. Such treatments which suppressed IFN-alpha/beta production did not influence bacterial growth in the organs of mice in the early stage of Listeria infection. Administration of IFN-alpha/beta exogenously also did not. After 5 days of infection when the specific resistance against reinfection with Listeria was established, IFN-gamma but not IFN-alpha/beta was induced in the circulation 3 to 6 hr after stimulation with LCWF or reinfection with Listeria. IFN-gamma production was abrogated completely by cyclophosphamide and antithymocyte serum, and partially by hydrocortisone and carrageenan, but not by anti-asialo GM1 antibody in Listeria-infected mice treated with these agents before induction of IFN-gamma by LCWF. Presumably, IFN-alpha/beta might be produced by asialo GM1-bearing cells but IFN-gamma might not. However, IFN-gamma production was suppressed in Listeria-infected mice, when IFN-alpha/beta production had been inhibited by treatment with anti-asialo GM1 antibody or when the IFN produced had been neutralized with anti-mouse IFN-alpha/beta antibody. Therefore, it is conceivable that IFN-alpha/beta might be essential for the generation or the expression of antigen-specific T cells involving IFN-gamma production and acquired resistance during Listeria infection. In fact, the bacterial growth in the organs of mice in the early stage of infection was normal in IFN-alpha/beta-depleted mice but it resulted in the delay of T-cell-dependent elimination of bacteria from the organs of mice in the late stage.

Animals↗
PubMed1984

Purification and properties of gene 18 product of bacteriophage T3.

Two noncapsid proteins of T3 and T7 phage, the products of gene 18(gp18) and gp19, are required for DNA packaging. By using in vitro complementation for DNA packaging as an assay system, T3 gp18 was purified to near homogeneity from an extract prepared cells infected with a mutant of gene 19(19- extract). The purified gp18 consisted of a single polypeptide having a molecular weight of 10,000, and was eluted as dimers and higher multimers from Sephadex G-75 columns. T7 gp18 was purified by the same procedures as that for T3 gp18 and behaved in the same manner as T3 gp18 throughout all purification steps. Gp18 from either T3 or T7 phage complemented both T3 and T7 18- extract for DNA packaging. These results indicate that, in contrast to gp19 [H. Fujisawa and M. Yamagishi (1981) Prog. Clin. Biol. Res. 64, 239-252], gp18 does not have specificity for T3 or T7 DNA during the in vitro packaging reaction. T3 gp18 was purified from extract containing functional gp19. The gp18 copurified with the gp19 activity. Gp18 and gp19 activities were stable when they were copurified but were unstable when purified separately. These results suggest that gp18 and gp19 function as a complex in the DNA packaging process. The gp18-gp19 preparation had a prohead-stimulated, DNA-dependent ATPase activity.

Adenosine Triphosphatases↗
PubMed1984

Oligo-2',5'-adenylate synthetase activity in peripheral blood mononuclear leukocytes in various diseases.

Interferon induces oligo-2',5'-adenylate synthetase in cells. In various diseases, interferon was detectable in the circulation or was produced spontaneously from peripheral blood mononuclear leukocytes. The oligo-2',5'-adenylate synthetase activity in peripheral blood mononuclear leukocytes was examined in various diseases, including systemic lupus erythematosus, sarcoidosis, Vogt-Koyanagi-Harada disease, and Behcet's disease. The activity of this enzyme was significantly increased in systemic lupus erythematosus (P less than 0.01), sarcoidosis (P less than 0.01), and Vogt-Koyanagi-Harada disease (P less than 0.01) compared with that in controls, but the increase of activity was not significant in Behcet's disease (P greater than 0.05).

2',5'-Oligoadenylate Synthetase↗
PubMed1983

Structural features of very fast sedimenting DNA formed by gene 49 defective T4.

Very fast sedimenting DNA (VFS DNA) of T4 phage, which is formed by infection with a mutant in gene 49, was examined by electron microscopy after mild treatment with DNase I. It showed Y-shaped, branched strands in addition to linear strands. Each branch contained a single-stranded interruption about 60 nucleotides long at its proximal end. The average number of branches per T4 DNA unit was close to the average number of sites susceptible to gene 49 nuclease. Both numbers were consistently changed by the addition of a secondary mutation in a gene involving recombination.

Centrifugation, Density Gradient↗
PubMed1983

Alternative induction of alpha/beta interferons and gamma interferon by listeria monocytogenes in mouse spleen cell cultures.

Production of interferon (IFN) by Listeria monocytogenes (LM) in nonimmunized mouse spleen cell cultures was studied. IFN-gamma defined by virtue of its acid stability and antigenicity was produced in spleen cell cultures obtained from ddY mice, C57BL/6 mice, and BALB/c mice in response to heat-killed (HK) LM within 24 hr. On the other hand, production of IFN-alpha/beta was demonstrated in spleen cell cultures obtained from one of four nude mice (BALB/c, nu/nu). Therefore, it is important to know the reason why the spleen cells of mice other than nude mice did produce only IFN-gamma, but did not produce IFN-alpha/beta in response to HK-LM. Spleen cells obtained from ddY mice were fractionated, and the cellular source for IFN production of either IFN-alpha/beta or IFN-gamma induced by HK-LM was investigated. IFN-gamma was produced only by a mixture of T lymphocytes (nylon wool-nonadherent, Thy-1-positive cells) and macrophages by HK-LM. Neither T lymphocytes nor macrophages alone produced IFN by HK-LM. Macrophage-depleted spleen cells produced neither IFN-gamma nor IFN-alpha/beta, but these cells acquired the ability to produce IFN-alpha/beta, not IFN-gamma, only when they had been treated with IFN-alpha/beta. A possible mechanism of both IFN-gamma and IFN-alpha/beta induction by Listeria in mouse spleen cell cultures is discussed.

Animals↗
PubMed1983

Effect of hypothalamic cooling on the tonic vibration reflex of gastrocnemius muscle in cats.

The tonic vibration reflex (TVR) in a medial gastrocnemius muscle (MG) was analyzed in 28 cats anesthetized with pentobarbital sodium while the preoptic-anterior hypothalamic region (PO-AH) was locally cooled or warmed in a thermoneutral environment. Cooling of the PO-AH did not produce shivering or changes in rectal and skin temperatures, but it brought about facilitation (16/28 cats) or inhibition (9/28) of the TVR in the MG. A few cats (3/28) showed inconsistent alteration of the TVR. Warming of the PO-AH did not produce any changes in the TVR of the MG. Histological identification of thermode placements revealed that in cats having the facilitatory response of the TVR, the thermodes were localized at regions caudal to A 14.0 mm and most of the thermodes in those having the inhibitory response were rostral to A 14.0 mm, except for two cases. Bilateral microinjection of a small quantity of anesthetic agent into the medial forebrain bundle (MFB) at the level of the mamillary body abolished the facilitatory effect of PO-AH cooling on the TVR. The results suggest that the spinal motor system is influenced by the PO-AH's sensitivity to local temperature and that the MFB constitutes part of the efferent pathway of the hypothalamic influence.

Animals↗
PubMed1983

Role of gene 8 product in morphogenesis of bacteriophage T3.

The product of gene 8 (gp8) of T3 phage is one of the minor head proteins located at the phage head-tail junction. To determine the role of gp8, an amber (8-) and four temperature-sensitive mutants (ts8) were characterized by sedimentation analysis, polyacrylamide gel electrophoresis, and extract complementation. Neither DNA-containing particles nor empty particles were formed in cells infected with 8-. In addition, prohead assembly was greatly reduced. Prohead assembly was also blocked in cells infected with all ts8 mutants at 42 degrees and with some ts8 even at 37 degrees. Proheads containing gpts8 were converted to empty heads when cell lysates were treated with chloroform. The protein compositions of proheads showed that the minor head proteins, gp8, gp15, and gp16, were lost from proheads formed in cells infected with ts8, but these minor proteins were present in proheads formed in cells infected with double mutants of ts8 and 5- or 19-, which are defective in DNA synthesis or DNA maturation, respectively. In vitro complementation experiments suggested that a ts mutation in gene 8 affected not only DNA packaging but also subsequent assembly steps. From these results, it is concluded that gp8 plays multiple roles in T3 phage morphogenesis, including prohead assembly, prohead stabilization, DNA packaging, and subsequent events.

Centrifugation, Density Gradient↗
PubMed1983

Involvement of gene 49 in recombination of bacteriophage T4.

The role of T4 gene 49 in recombination was investigated using its conditional-lethal amber (am) and temperature-sensitive (ts) mutants. When measured in genetic tests, defects in gene 49 produced a recombination-deficient phenotype. However, DNA synthesized in cells infected with a ts mutant (tsC9) at a nonpermissive temperature appeared to be in a recombinogenic state: after restitution of gene function by shifting to a permissive temperature, the recombinant frequency among progeny increased rapidly even when DNA replication was blocked by an inhibitor. Growth of a gene 49-defective mutant was suppressed by an additional mutation in gene uvsX, but recombination between rII markers was not.

DNA, Viral↗
PubMed1983

Spontaneous production of gamma-interferon in cultures of T lymphocytes obtained from patients with Behçet's disease.

The spontaneous production of interferon (IFN) in the cultures of peripheral blood mononuclear leukocytes (PBML) obtained from 30 patients with Behçet's disease was investigated. PBML obtained from each of 26 patients in the convalescent stage and four patients in the exacerbation stage were cultured at least twice without stimulation, and IFN activity in the culture fluid 2 to 7 days after the cultivation was assayed. Twenty PBML of normal healthy donors were also cultured simultaneously. PBML of all patients in the convalescent stage spontaneously produced high-titered IFN (60.0 +/- 9.5 IU/ml), but IFN activity produced in PBML cultures of four patients in the exacerbation stage was very low or was undetectable. Similarly, IFN was always detectable in the circulation of the patients whose PBML spontaneously produced IFN. All IFN activity detected both in the circulation and in the fluid of PBML culture from these patients was gamma-IFN, defined by virtue of its acid lability and antigenicity neutralized with antiserum for gamma-IFN and not with antisera for alpha- and beta-IFN. The cellular source of this gamma-IFN in the patients' PMBL was T lymphocytes and not non-T cells or macrophages. T lymphocytes did not require the help of macrophages. It is suggested that T lymphocytes of these patients may be stimulated by unknown causative agents in vivo and may produce gamma-IFN in vivo as well as in in vitro culture of T lymphocytes.

Adult↗
PubMed1982

Detection of gamma interferon in the sera of patients with Behçet's disease.

The serum levels of interferon (IFN) in 58 patients with Behçet's disease were significantly higher than those in 79 normal controls (P less than 0.0001). The average IFN titer was 51.4 +/- 9.3 IU/ml in the patients and 5.9 +/- 1.1 IU/ml in the controls. The patients were then divided into two groups according to the stage of ocular disease. Forty-six patients in the ocular convalescent stage had higher IFN levels (61.3 +/- 11.2 IU/ml) than did 12 patients in the exacerbation stage (13.2 +/- 3.0 IU/ml). Moreover, the kinetics of the IFN level in the circulation of seven patients showed a significant decrease of IFN in the exacerbation stage. IFN activity in sera from patients was destroyed by acid treatment and heating at 56 degrees C for 30 min and was not neutralized with anti-human IFN-alpha and -beta sera. In addition, it was demonstrated that vesicular stomatitis virus inhibitors detected in sera from both the patients and the controls had no effect on our IFN assay. Therefore, antiviral activity detected in sera of patients seems to be due to gamma interferon (IFN-gamma). IFN-gamma may play a significant role in the pathophysiology of Behçet's disease.

Adolescent↗