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M Sasano

Publications and source records attributed to M Sasano.

32 records · Page 2Linked to original sources
PubMed1990

Production of prostaglandin E2 induced by histamine by cloned rheumatoid synovial cells.

Production of prostaglandin E2, with or without histamine stimulation, by three different types of cloned rheumatoid synovial cells (macrophage like, dendritic, and fibroblast like) was evaluated. The ability of these cloned cells to respond to histamine on a cell to cell basis was as follows: macrophage like cells responded most strongly, followed by dendritic cells, followed by fibroblast like cells. Production of prostaglandin E2, stimulated by histamine, may have a role in bony destruction in rheumatoid joints.

Adult↗
PubMed1990

Adherent synovial cells from nonrheumatoid arthritis do not release interleukin 1 beta and prostaglandin E2 spontaneously in longterm culture.

Adherent synovial cells from both 13 patients without rheumatoid arthritis (RA) (gout, osteoarthritis and meniscal lesion) and 8 patients with RA consisted of dendritic cells, macrophage-like cells and fibroblast-like cells after cloning in a similar fashion as reported in our previous paper. All the adherent synovial cells from patients without RA did not release interleukin 1 (IL-1) beta and prostaglandin E2 (PGE2) spontaneously, while those cells released comparable amounts of IL-1 beta, but not PGE2 to RA cells after type II collagen stimulation. Only the synovial cells from RA, irrespective of morphology and cloning, released IL-1 beta and PGE2 without stimulation. Nonrheumatoid synovial cells may differ functionally from RA cells.

Arthritis, Rheumatoid↗
PubMed1989

Decrease in disease activity and concomitant increase in the percentage of peripheral blood suppressor T-cells in rheumatoid arthritis by a newly synthesized slow-acting anti-rheumatic drug (Bucillamine).

Bucillamine: N-(2-mercapto-2-methyl-propanoyl)-L-cysteine, is a newly synthesized slow-acting anti-rheumatic drug with two SH-bonds in its chemical structure. Eleven patients with rheumatoid arthritis (RA) were treated with Bucillamine, and both Lansbury's activity index and the percentage of suppressor T-cells (Leu 2a+ Leu 15+) were serially monitored for 10 weeks. The percentage of suppressor T-cells, which was depressed in the active disease state, reached normal levels with clinical improvement according to Lansbury's index. Bucillamine may have an immunomodulating activity and may be a useful drug for the treatment of RA.

Adult↗
PubMed1989

Lack of association of HLA-DR4 with interleukin 1 beta secretion from peripheral blood monocytes in patients with rheumatoid arthritis.

The possible association between HLA-DR4 and interleukin 1 beta (IL-1 beta) secretion from peripheral blood monocytes was analyzed using 34 female patients, with definite rheumatoid arthritis (RA). RA monocytes in serum-free medium or medium supplemented with 10% fetal calf serum secreted IL-1 spontaneously. The level of secretion was enhanced by stimulation with pyrogen-free type II collagen as determined by comparison with 30 healthy individuals matched for age and sex. No association between HLA-DR4 and spontaneous or stimulated IL-1 release from RA monocytes was observed.

Adult↗
PubMed1988

Augmented interleukin-1 production and HLA-DR expression in the synovium of rheumatoid arthritis patients. Possible involvement in joint destruction.

Potent interleukin-1 (IL-1) activity was detected in culture supernatants from synovium, obtained by arthroscopy, from rheumatoid arthritis (RA) patients but not from non-RA patients. Production of IL-1 by RA synovium correlated well with findings of inflammation on arthroscopy and HLA-DR expression in immunohistochemical staining. Furthermore, there was a positive correlation between IL-1 production from RA synovium and joint changes detected on roentgenograms. These findings strongly suggest that IL-1 might play an important role in the joint destruction in RA.

Adult↗
PubMed1988

Stimulation of interleukin-1 alpha and interleukin-1 beta release from human monocytes by cyanogen bromide peptides of type II collagen.

Pyrogen-free cartilage fragments from patients with fracture, osteoarthritis, or rheumatoid arthritis were found to stimulate the production of interleukin-1 alpha-like and interleukin-1 beta-like factor by peripheral blood mononuclear cells from healthy individuals and rheumatoid arthritis patients. The stimulatory cartilaginous component was type II collagen, and the major stimulatory determinant on type II collagen was found to be cyanogen bromide 11 peptide. These results suggest a possible pathogenic role of the intact cartilaginous component in interleukin-1-mediated joint destruction.

Arthritis, Rheumatoid↗
PubMed1988

pH dependency of effect of topically applied dipivefrine hydrochloride on intraocular pressure and pupil size in rabbits: comparative studies with epinephrine.

The pH and dose dependencies of topically applied dipivefrine hydrochloride (DPE) on intraocular pressure (IOP) reduction and mydriasis were compared with those of epinephrine bitartrate (EPI) in normal rabbits. Statistically significantly greater IOP lowering and mydriatic effects of DPE solutions were achieved by increasing their pH from 3 to 6 or their concentrations from 0.02% to 0.1%. The ocular hypotensive and mydriatic effects of EPI also depended on their concentrations, but not on their pH. On the other hand, blink rates of rabbits following topical application of DPE tended to be reduced by the increase of pH, while they were not influenced by the concentrations. From these results, it was indicated that the pharmacological effects of DPE were augmented about 3 times by increasing the pH of its solutions from 3 to 5, which also was associated with reduction of ocular irritation, while the effects of EPI were not altered by the changes of pH. As the result of the increase of pH from 3 to 5, DPE became about 50 times more potent than EPI as a ocular hypotensive agent.

Administration, Topical↗
PubMed1987

Spontaneous production of an interleukin 1-like factor by cloned rheumatoid synovial cells in long-term culture.

We have cloned adherent synovial cells from rheumatoid synovitis. These can be generally divided into three types, including cells that have the characteristic features of dendritic cells (DCs), macrophagelike cells (MCs) and fibroblastlike cells (FCs), as classified by morphology and immunofluorescent staining. The cloned cells were able to divide and were cultured for up to 11 mo without any significant morphological changes. All the cloned cells were HLA-DR+ after gamma-interferon treatment. Spontaneous production of a factor with interleukin 1 activity by the cloned cells was detected even after long-term culture (the ability, on a per cell basis, being in the following order: DC greater than MC greater than FC). These synovial cells may be important for bony destruction in rheumatoid joints.

Arthritis, Rheumatoid↗
PubMed1986

In vitro generation of antigen-specific suppressor T cell activity. Culture conditions for abrogating the induction of nonspecific suppressor T cells.

When murine lymphocytes were cultured in RPMI-1640 medium containing fetal calf serum (FCS) for more than 3 d without added antigens, suppressor T cells (Ts) that suppressed in vitro antibody responses to sheep erythrocytes, dinitrophenyl-Ficoll and trinitrophenyl (TNP)-lipopolysaccharide nonspecifically were induced spontaneously. Thus, we failed to detect the activities of antigen-specific Ts that are generated by priming the lymphocytes in vitro with a specific antigen under these experimental conditions. To avoid the induction of nonspecific Ts, we examined various culture conditions and found that nonspecific Ts were not induced only when a specific lot of FCS (NSF 107) was used. When the lymphocytes were cultured with Keyhole limpet hemocyanin (KLH) in NSF 107-containing culture medium, we could detect KLH-specific Ts activity that specifically suppressed the secondary response to TNP-KLH without the interference of nonspecific Ts. Similar experiments were successful if we used FCS that was previously treated at 70 degrees C for 10 min instead of native ones. Immunoelectrophoretic analysis revealed that the level of a component belonging to alpha-globulin fraction was markedly low in NSF 107 as compared with all other lots of FCS that could induce nonspecific Ts. Removal of this component from FCS by an immunoadsorbent resulted in the loss of capacity to induce nonspecific Ts. On the other hand, when the lymphocytes were cultured in the presence of varying amounts of this component, nonspecific Ts were generated in a dose-dependent manner.

Animals↗
PubMed1985

[Pharmacological studies on N-(2-mercapto-2-methylpropanoyl)-L-cysteine(SA96). IV. Effects of SA96 and its main metabolite, SA679, on denaturation of human gamma-globulin and adjuvant arthritis in rats].

SA96 and its main metabolite, SA679, were investigated for their effects on denaturation of human gamma-globulin and bovine serum albumin (BSA) and on adjuvant arthritis in Lewis rats. The heat denaturation of human gamma-globulin and BSA enhanced by Cu2+ was inhibited by SA96, SA679 and D-penicillamine, and the inhibitory effect of SA96 was the most potent. In adjuvant arthritis rats, SA96 given orally at a dose of 10 mg/kg from the same day as the adjuvant injection inhibited significantly the swelling of adjuvant treated foot and untreated foot, increase of the relative organ weights of the adrenals, liver and kidney, and increase of serum Cu concentration; but at a dose of 100 mg/kg, it did not show any effects on these parameters. On the other hand, SA96 given from three days before the adjuvant injection showed the inhibitory effects at a dose of 100 mg/kg as well as 10 mg/kg. These results suggest that the effect of SA96 on adjuvant arthritis in rats depends on its administration schedule. SA679 also inhibited the adjuvant arthritis at a dose of 100 mg/kg, but its effect was less potent than that of SA96.

Animals↗
PubMed1983

Effect of N-(2-carboxyphenyl)-4-chloroanthranilic acid disodium salt (CCA) on the induction of helper and suppressor T cells in vitro and in vivo.

Keyhole lympet hemocyanin (KLH)-specific suppressor T (Ts) cells that suppress the in vitro secondary anti-trinitrophenyl (TNP) PFC response to TNP-KLH could be induced when murine spleen cells were precultured with KLH. N-(2-carboxyphenyl)-4-chloroanthranilic acid disodium salt (CCA) at 1-100 micrograms/ml augmented the in vitro induction of Ts cells when the cells were precultured with a suboptimal dose of KLH (10 micrograms/ml). Ts cell-induction was, however, rather slightly inhibited by the same concentrations of CCA when the lymphocytes were precultured with an optimal amount of KLH (100 micrograms/ml). In the in vivo experiments, the daily administration of 10 mg/kg CCA for 4 weeks augmented or inhibited Ts cell-induction when mice were immunized with a suboptimal (30 micrograms/body) or an optimal (100 micrograms/body) amount of KLH, respectively. However, CCA had no effect on the induction of Ts cells by concanavalin A in vivo. On the other hand, CCA augmented the induction of helper T (Th) cells both in vitro and in vivo when Th cells were induced with a suboptimal amount of antigens. In contrast, the augmentative effect was no longer observed when Th cells were induced by an optimal amount of antigens. These results suggest that CCA is a compound showing immunomodulating properties that affect Ts and Th cell-induction depending on immunological conditions. These immunopharmacological profiles are discussed in connection with its clinical application to an autoimmune disease like rheumatoid arthritis.

Animals↗
PubMedDate not supplied

Protective effect of (4R)-hexahydro-7,7-dimethyl-6-oxo-1,2,5-dithiazocine-4-carboxylic acid (SA3443), a novel cyclic disulfide, on immunologically induced liver injuries in mice.

The effects of (4R)-hexahydro-7,7-dimethyl-6-oxo-1,2,5-dithiazocine-4- carboxylic acid (SA3443), a novel cyclic disulfide, on new immunological liver injury models were investigated. The first liver injury model included a single injection of rabbit anti-basic liver protein antibody into DBA/2 mice. Serum transaminase activities showed a dose-dependent increase 42 hr after the antibody treatment. SA3443 significantly inhibited the elevation of serum transaminase activity and the histopathological changes of the liver in antibody-treated mice at doses of 100 to 300 mg/kg, p.o. The second hepatic failure model was based on an injection of lipopolysaccharide into BALB/c mice which had been previously treated with heat-killed Propionibacterium acnes (P. acnes). SA3443 reduced the lethal acute hepatic failure at doses of 100 to 300 mg/kg. Moreover, a distinct increase in lymphocyte-activating factor activity was detected in the supernatant of the culture medium of the liver macrophage/Kupffer cells isolated from the rat treated with P. acnes. SA3443, at 10(-6) to 10(-4) M, suppressed the release of the lymphocyte-activating factor activity from liver macrophage/Kupffer cells. These results suggest that SA3443 provides considerable protection against immunological liver injuries, and that the efficacy of SA3443 might be partially related to an inhibition of the increase in lymphocyte-activating factor activity.

Alanine Transaminase↗