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Biomedical subjects

K Kakimoto

Publications and source records attributed to K Kakimoto.

At least 73 records · Page 4Linked to original sources
PubMed1989

Effect of freeze-thawing breast milk on vertical HTLV-I transmission from seropositive mothers to children.

Breast feeding is known to be a major cause of vertical transmission of HTLV-I from mothers to her children. The infectiousness of HTLV-I in breast milk was reported to be lost during freezing and thawing processes. We therefore administered frozen-and-thawed breast milk of HTLV-I carriers to their babies. Among the 13 babies given the frozen-and-thawed breast milk (now 12 months of age), no infection has been found yet. This result suggests that freezing and thawing of breast milk is a promising method for the prevention of vertical HTLV-I infection to breast-fed babies.

Breast Feeding↗
PubMed1989

Signal delivery by physical interaction and soluble factors from accessory cells in the induction of receptor-mediated T-cell proliferation. Synergistic effect of BSF-2/IL-6 and IL-1.

Our recent study revealed that soluble factors derived from accessory cells (AC; monocytes) and physical interaction with T cells of the accessory cells are both required for the induction of the proliferation of human peripheral blood T cells by anti-CD3 antibody coupled on latex beads. The accessory cell-derived soluble factor could be replaced by IL-1 and IL-6, and the role of live macrophages for physical interaction with T cells was found to be replaceable with paraformaldehyde(PFA)-fixed macrophages, provided the macrophages were pretreated with interferon-gamma (IFN-gamma) before fixation. Quantitative analysis in the present study revealed that IL-1 and IL-6 act synergistically to induce T-cell proliferation in the above system but either one of the factors alone reveals only a marginal or weak activity. Furthermore, it was shown that the potentiating activity of the culture supernatants of monocytes was substantially inhibited by anti-IL-6 antibody. Taken together with our previous results that anti-IL-1 serum strongly inhibited the potentiating activity of the culture supernatant, these results indicate that the main responsible molecules in the culture supernatant are IL-1 and IL-6, although a presence of other effective factors is not excluded. The anti-CD3-induced thymidine uptake by T cells in the presence of IL-1 and IL-6 was significantly inhibited by anti-Tac antibody, suggesting that the proliferation of T cells in this system is mostly mediated by a IL-2-dependent pathway. Our study further showed that accessory cells seem to acquire cell surface properties necessary for the effective interaction with T cells during 6-24 hr of culture with IFN-gamma. Presumably, a certain molecule(s) required for the interaction is induced on the cell surface of the AC by IFN-gamma.

Antibodies, Monoclonal↗
PubMed1988

Induction of an anti-human type II collagen response by monoclonal anti-idiotypic antibody.

Several distinct epitopes on human type II collagen were defined by using mAb. The presence of species-specific and species-nonspecific (common) epitopes was thus clarified. Anti-idiotypic mAb (Ab2) was developed against one of the antibodies (Ab1) reactive with species-specific epitopes. Thus Ab2 was demonstrated to recognize an idiotope expressed on the Ag-binding site (paratope) of Ab1, since the binding of Ab1 to human type II collagen was blocked by Ab2, and the binding of Ab2 to Ab1 was inhibited by soluble human type II collagen, but not by murine and bovine type II collagens. DBA/1 mice immunized with Ab2 coupled to keyhole limpet hemocyanin produced an antibody (Ab3) specifically reactive with human type II collagen. It was also demonstrated that Ab3 expressed an idiotype similar to that of Ab1. These findings indicate that anti-idiotypic antibody directed against mAb to human type II collagen mimics a species-specific epitope on human type II collagen. The anti-idiotypic antibody bearing internal image of type II collagen will open the way to isolation of the arthritogenic epitope on type II collagen.

Animals↗
PubMed1988

Isolation of T cell line capable of protecting mice against collagen-induced arthritis.

A T cell line specific to human type II collagen (CII) was selected and propagated from DBA/1J mice immunized with human CII. The line cells were not reactive to type I or type III collagen of human origin, but they were cross-reactive to bovine, rat, and rabbit CII and they recognized both native and heat-denatured human CII. The cells were reactive to an N-terminal three-quarters fragment of human CII, produced by tadpole collagenase digestion of human CII, but not to a C-terminal one-quarter fragment of human CII. The cells showed Thy-1+, Lyt-1+, Lyt-2-, and L3T4+ phenotypes characteristic of T helper cells or delayed-type hypersensitive cells, determined by the immunofluorescence method. To clarify the role of T cells in the pathogenesis of collagen-induced arthritis, we inoculated this cell line into DBA/1J mice and found that they developed clinical arthritis, albeit at a low incidence. The cells attenuated by x-ray were capable of inducing resistance to the subsequent induction of collagen-induced arthritis of DBA/1J mice. The sera from mice protected by inoculation of the cell line exhibited anti-idiotypic antibody response against conventional and monoclonal anti-CII antibodies. Anti-T cell receptor response may be involved in the mechanism for the protective effect of the cell line against autoimmune murine arthritis.

Animals↗
PubMed1988

Thymic accessory cells required for the increased responsiveness of thymocyte subpopulations to interleukin 1-like monokine in guinea pigs.

The proliferative response of guinea-pig thymocytes to co-mitogenic stimulation with phytohaemagglutinin and the guinea-pig interleukin 1 (IL-1)-like lymphocyte-activating monokine was lost by removing the cells that adhere to a Sephadex G-10 (G-10) column or the cells of low density in a Ficoll-Conray gradient. The diminished response in the G-10 non-adherent thymocyte or high-density thymocyte fraction was restored by the addition of a macrophage-depleted G-10 adherent thymocyte fraction or a low-density, Ia-positive thymocyte fraction but not by the addition of peritoneal macrophages. These results suggest that the accessory cells which mediate the increased responsiveness of thymocytes to the IL-1-like monokine existed in G-10 adherent cell fractions and the cells with this accessory function were not macrophages. The accessory cells were shown to be of low density, glass-non-adherent, G-10-adherent, Fc receptor-negative, and Ia-positive. These results also suggest that the G-10-non-adherent and high-density thymocyte subpopulation, which is unresponsive or responds very little to the IL-1-like monokine by itself, acquires responsiveness to the monokine and proliferates by stimulation with the IL-1-like monokine and lectin in the presence of the accessory cells.

Animals↗
PubMed1987

Induction of delayed-type hypersensitivity by the T cell line specific to bacterial peptidoglycans.

A T cell line specific for the chemically well-defined peptidoglycan of bacterial cell wall, disaccharide tetrapeptide, was established from Lewis rats immunized with the antigen covalently linked to the autologous rat serum albumin. The antigen specificity was examined with various analogues or derivatives of the peptidoglycan. The cell line was reactive to analogues with the COOH-terminal D-amino acid, but least reactive to those with L-amino acid as COOH terminus. Transferring of the T cell line into X-irradiated normal Lewis rats induced delayed-type hypersensitivity in an antigen specific manner.

Animals↗
PubMed1987

[Study on Na+ and L-alanine cotransport of the human placenta using microvillous membrane vesicles].

Using microvillous membrane vesicles prepared from human normal term placenta, placental cotransport system of Na+ and L-alanine was studied using rapid filtration technique. The uptake of L-alanine into microvillous membrane vesicles was Na+ ion electrochemical gradient (extravesicular greater than intravesicular) dependent and showed typical overshoot phenomenon. Both Na+ dependent L-alanine uptake and Na+ ion uptake into microvillous membrane were membrane potential dependent and were markedly increased when the intravesicular space was rendered electrically more negative by membrane diffusion potentials, induced by the use of highly permeant anions. L-alanine gradient (extravesicular greater than intravesicular) induced a temporary accumulation of Na+ ions. These results indicated that L-alanine and Na+ ions were cotransported across microvillous membrane and this cotransport was dependent on the electrical potential difference in the membrane.

Alanine↗
PubMed1986

Combined mutagenicity of cobalt(II) salt and heteroaromatic compounds in Salmonella typhimurium.

Mutagenic activities of 4-aminopyridine (4AP), 4-aminoquinoline (4AQ), 9-aminoacridine (9AA) and harman (HM) were examined by the Salmonella test system in the presence of cobalt(II) chloride (CoCl2), which itself is non-mutagenic in this system. Mutagenic activity of the mixture of 9AA and CoCl2 was found to be much higher than that of 9AA alone in strains TA1537 and TA2637. A similar enhancing phenomenon was observed in 4AQ-CoCl2 and HM-CoCl2 mixtures but not in that of 4AP-CoCl2. Judging from visible and nuclear magnetic resonance spectral data, this increased mutagenicity may be attributable to the formation of moderate to weak complexes between these chemicals and the Co(II) cation. A survey of the mutagenicity of several Co(II) complexes supported this interpretation.

Cobalt↗
PubMed1986

Muramyl dipeptide induces acute joint inflammation in the mouse.

Acute joint inflammation was produced in BALB/c mice by a single intravenous injection of synthetic muramyl dipeptide (MDP), its stereoisomers and 6-O-acyl derivatives of MDP. Four adjuvant-active, but not five adjuvant-inactive MDP analogs induced acute swelling and erythema of the ankles and wrists which were detected around 6-10 hr, reached the maximum severity by 18-24 hr and subsided by days 3 to 4 after injection. Introduction of the stearoyl group, but not the alpha-branched long chain fatty acid group into the C-9 hydroxyl group of MDP enhanced and prolonged the joint lesions compared with MDP.

Acetylmuramyl-Alanyl-Isoglutamine↗
PubMed1985

Acute joint inflammation in mice after systemic injection of the cell wall, its peptidoglycan, and chemically defined peptidoglycan subunits from various bacteria.

The systemic injection of an aqueous suspension of cell wall or its peptidoglycan (PG)-rich sonicate derived from group A streptococcus and Lactobacillus casei induced acute joint lesions in BALB/c, DBA/1J, (BALB/c X DBA/1J)F1, and C3H/He mouse strains, but not in C57BL/6, DBA/2, and AKR strains. Cell walls and their enzymatically degraded PG fragments from other bacteria as well as the synthetic disaccharide dipeptide and Lactobacillus plantarum cell wall-derived disaccharide tripeptide produced similar acute inflammation in susceptible BALB/c mice. Acute swelling and erythema of the ankles and wrists were observed as early as 3 h, reached maximum severity by day 2, and generally subsided by days 4 to 6 after injection. Histological studies showed synovial proliferation, marked infiltration of many mononuclear cells and a few polymorphonuclear leukocytes in the soft tissues, and extensive deposition of fibrinous exudate in the joint space. Antibody response was detectable against the PG fraction. However, anti-PG antibody does not seem to be responsible for the pathogenesis of this disease. On the other hand, experiments on decomplementation by cobra venom factor suggest that complement components are involved in the early phase of this arthritic model.

Animals↗
PubMed1985

Characterization of monoclonal antibody specific for human type II collagen: possible implication in collagen-induced arthritis.

We obtained monoclonal antibodies specific for human type II collagen and characterized them using human collagen type I, II, III and V and tropocollagen A (3/4) (TCA) and tropocollagen B (1/4) (TCB) fragments of type II collagen which were obtained by digestion with tadpole collagenase. These antibodies were of the IgG2a class and specific for the conformational determinant of TCA fragment of type II collagen. When injected intravenously into DBA/1J mice, one of the monoclonal antibodies induced arthritis, which was characterized by early onset, mildness in severity and preferential localization mainly in the peripheral joints of the lower extremities. These results suggest that, at least, one of the arthritogenic determinants of type II collagen for collagen-induced arthritis of mice exists in the three quarter region from the N-terminus of type II collagen.

Animals↗
PubMed1984

Structure-dependent variation in the mutagenic, prophage-inducing and antibacterial activities of 5-nitro-2-furamide derivatives.

A comparative survey of the mutagenic, prophage-inducing and antibacterial activities of 3 structure-related series of 5-nitro-furan derivatives including 5-nitro-2-furohydrazide imide, 5-nitro-2-furamide oxime and 5-nitro-2-furohydrazide has been undertaken. Among the compounds assayed, the 5-nitro-2-furohydrazide imide series was found to be most active with regard to mutagenic and antibacterial activities against Salmonella typhimurium TA100 and prophage-inducing activity in Escherichia coli GY5027. A clear correlation was observed between the chemical structure and the mutagenic and prophage-inducing activities which were approximately correlated to the antibacterial activity.

Anti-Bacterial Agents↗