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Biomedical subjects

I Morisaki

Publications and source records attributed to I Morisaki.

At least 55 records · Page 3Linked to original sources

Gingival overgrowth induced by cyclosporin A in rats.

Gingival overgrowth, which is one of the major side-effects of this immunosuppressive agent, was studied in specific pathogen-free Fischer rats fed diet No. 2000 containing 56% sucrose. Marked macroscopic overgrowth was noted in mandibular gingiva of all the rats fed this diet containing cyclosporin A. The overgrowth was more severe in buccal than in lingual gingiva. Rats fed the cyclosporin-containing diet and infected with Streptococcus sobrinus 6715 had the most gingival overgrowth. Histopathological examination revealed that the bulk of the enlargement consisted of fibrous connective tissue without a marked increase in the number of fibroblasts or inflammatory cells.

Animals↗

Complete root resorption of an upper central incisor due to ectopic eruption of canine in a deaf-mute child.

Unilateral complete root resorption of the permanent central incisor was experienced in a boy with deaf and dumb. Transposition of tooth germ or abnormally directed eruption of the canine caused not only an entire root but a part of enamel resorption. The patient was diagnosed clinically and radiographically as an ectopic eruption of the right maxillary upper canine and then treatments were provided to improve esthetic and functional conditions in terms of eruption guidance. It should be emphasized that the early diagnosis and the subsequent eruption guidance is essential in the patient with these kinds of eruption disorder of the mixed dentition.

Adolescent↗

Orofacial manifestations in a child with Fanconi's syndrome.

Orofacial and dental findings in a child with Fanconi's syndrome and accompanying glycogen storage disease are presented. Remarkable retardation of skeletal growth, resulting in dwarfism, was noted. Cephalometric analyses revealed that the size of the patient's craniofacial bones at 10 years of age was as small as that of the average 4-year-old child. Development of the permanent dentition was retarded for 3 to 4 years. Histologic examination of an exfoliated primary canine showed hypomineralization of the dentin structure.

Cephalometry↗

Vertical crown-root fracture of the mandibular first primary molar in a one-year-old child.

A vertical crown-root fracture of the mandibular first primary molar in a 21-month-old child is presented. The mandibular primary first molar was fractured vertically and split into 2 pieces. The tooth fracture had not been noticed for about 5 months after the accident, and the tooth was left without any treatment. The pulp tissue of the mesial root maintained its vitality, but the distal root was nonvital.

Humans↗

[Changes of antibody and splenic plaque forming cell responses to mutans streptococci in the rats infected with S. sobrinus 6715].

The study was undertaken to examine the changes in humoral IgM, IgG and IgA antibodies and splenic plaque forming cell responses against Streptococcus sobrinus 6715 in rats infected with the same mutans streptococci. The serum samples were collected every week for 24 weeks after infection (20 day old, Sprague Dawley rats). Humoral anti-S. sobrinus 6715 IgG and IgA antibodies were determined by an enzyme-linked immunosorbent assay. In the separate experiment, rat splenic IgM, IgG and IgA anti-trinitrophenyl (TNP) conjugated S. sobrinus plaque-forming cell (PFC) responses were also determined from 1 to 12 weeks after the infection. The results obtained were as follows: 1. From 1 to 4 weeks after infection, a slight increase in serum IgG anti-S. sobrinus antibody response was observed in the group of rats infected with S. sobrinus 6715 when compared with the non-infected rat group. However, beyond the 5th week, there was no difference in serum antibody responses between these two groups. 2. Infected rats showed a 2-9 times higher serum anti-S. sobrinus IgA antibody response than those of uninfected rats for 6 weeks after the infection. After this period just as with the IgG response, no difference in the IgA titers was found between these two groups. 3. Splenic IgM, IgG and IgA anti-TNP-S. sobrinus PFC responses showed a remarkable decrease shortly after the infection. These results suggest that the infected rats would gradually acquire oral tolerance to S. sobrinus antigen after the infection.

Animals↗

Corneal test as a reliable method for detection of the delayed-type hypersensitivity reaction in mice.

Antigen solution could be injected into the cornea of sensitized mice using a fine needle and a stereoscopic dissecting microscope. The resulting corneal reaction was shown to be a reliable method in the detection and estimation of delayed-type hypersensitivity in mice that had been immunized with a water-in-oil emulsion containing an ovalbumin and a cell wall adjuvant. Unlike the delayed skin reaction in the ear lobe, this corneal reaction was not affected by a coexisting Arthus reaction.

Animals↗

Cell wall preparation consisting of group A carbohydrate and peptidoglycan moieties from Streptococcus pyogenes activates murine B lymphocytes.

Cell walls from Streptococcus pyogenes strain Sv (Group A, M type 3) were lysed with M1 endo-N-acetylmuramidase, and the group A-specific carbohydrate antigen was purified by Sephadex G-100 gel filtration. The initial eluting antigen (M1gA) peak was assessed for mitogenic and polyclonal lymphocyte-activating properties in murine spleen cell cultures. Good mitogenic responses were induced over a broad dose range (1-100 micrograms) with M1gA in both BALB/c and C3H/HeJ splenic cultures. Similar mitogenic responses were induced in nude (nu/nu) and nu/+ splenic cultures, suggesting that M1gA is a B cell mitogen. The M1gA induced anti-trinitrophenyl, anti-sheep erythrocytes, and anti-horse erythrocytes polyclonal plaque-forming cell responses in splenic cell cultures. Studies with purified splenic B cells and M1gA suggest that the mitogenic responses were indeed thymic independent. These studies clearly indicate that native group A carbohydrate antigen is a B cell mitogen and polyclonal B cell activator.

Animals↗

Immunoregulation in the rat: ontogeny of B cell responses to types 1, 2, and T-dependent antigens.

The development of rat B cells has been examined in neonatal and adult Fischer rats through the use of type 1 (TNP-Brucella abortus), type 2 (TNP-LPS(Ph), TNP-Ficoll) and T cell-dependent (TD) (SRBC) antigens. In vivo splenic PFC responses to TNP-Brucella abortus could be induced in newborn rats and by 12 days of age had reached adult levels. In contrast, the responses to the type 2 and TD antigens were 30% and 70%, respectively, of the adult levels at 30 days of age. Adoptive transfer of the B cells from neonatal and young rats into irradiated adult hosts demonstrated that the kinetics in the development of responses to these antigens (early for type 1, intermediate for TD, and late for type 2) were not due to limiting accessory cell or T cell help in immature rats. In vitro cultures of purified B cells from neonatal and adult rats were responsive to TNP-BA and TNP-LPS(Ph) but not to TNP-Ficoll and SRBC. However, the addition of spleen cell-derived Con A supernatant to the B cell cultures resulted in responses to all four antigens, which arose as a function of B cell age, with kinetics that were identical to those observed in vivo. Fluorescent staining of B cells from rats of various ages for cell surface IgM and analysis on the fluorescence-activated cell sorter (FACS) revealed that all splenic B cells from rats 4 days of age expressed a relatively high level of sIgM, and that a subpopulation that expressed a relatively low level of sIgM increased with age until it represented approximately 50% of the adult splenic B cells. Challenging Con A supernatant-supplemented cultures of FACS-prepared low sIgM+ and high sIgM+ cells revealed that B cells responsive to TNP-Ficoll were confined to the ontogenically late-arising low sIgM+ subpopulation but that B cells responsive to TNP-BA, TNP-LPS(Ph), and SRBC were present in both subpopulations.

Aging↗

Immunoregulation in the rat: cellular and molecular requirements for B cell responses to types 1, 2, and T-dependent antigens.

The requirements for primary in vitro plaque-forming cell (PFC) development in cultures of purified rat splenic B cells have been examined. Rat B cells were directly responsive to the type 1 antigen trinitrophenyl-Brucella abortus (TNP-BA), but both T cells and adherent accessory cells were required for B cell responses to the type 2 antigen TNP-Ficoll and the T cell-dependent (TD) antigen sheep erythrocytes (SRBC). However, the cellfree supernatants from concanavalin A-induced spleen cells of rat or mouse origin replaced the requirement for T cells and macrophages, and resulted in PFC development in response to TNP-Ficoll and SRBC and augmented PFC numbers in response to TNP-BA. Culture supernatants from induced murine T cell and macrophage cell lines were used to partially deduce the molecular requirements for the support of PFC development by rat B cells to these three antigens. Supernatants from the EL-4 (EL-4 sup) and B151 K12 (B15 sup) T cell lines augmented TNP-BA responses, suggesting that B cell growth factor II (BCGF-II) mediated this effect. An admixture of purified interleukin 2 (IL 2) and B15 sup supported PFC development to SRBC; indicating that IL 2, BCGF-II, and the T cell-replacing factor in B15 sup (B15-TRF) were sufficient to support this response. In addition, the IL 2 plus B15 sup-supported anti-SRBC PFC response was increased by the addition of an interleukin 1-containing fraction from the supernatant of the macrophage line P388D1. PFC development in response to TNP-Ficoll had the most stringent requirements and only occurred in the presence of EL-4 sup and B15 sup (IL 2, BCGF-I, BCGF-II, EL-TRF, B15-TRF). These data indicate that different cellular and molecular requirements exist for PFC development in response to types 1, 2, and TD antigens by rat B cells.

Animals↗

An enzyme-linked immunosorbent assay (ELISA) for quantification of antibodies to Streptococcus mutans surface antigens.

An ELISA was developed to quantitate the level of antibodies to various cell surface antigens of the Gram positive bacterium, Streptococcus mutans. Whole cells and purified cell wall components of S. mutans, lipoteichoic acid (LTA) from Streptococcus pyogenes, and dextran T 2000 were employed as coating antigens in this study. Cell walls of S. mutans were purified by mechanical disruption of whole cells followed by differential centrifugation and proteolytic enzyme treatment. Serotype-specific carbohydrate was purified from an autoclaved, lyophilized S. mutans whole cell preparation by column chromatography. LTA was prepared by Sepharose 4B chromatography of a phenol-water extract of S. pyogenes and used for detection of anti-polyglycerophosphate (PGP) antibodies. A rabbit antiserum to S. mutans 6715 (serotype g), which precipitated with purified carbohydrate antigen (RR g), gave good reactions with purified cell walls and whole cells of S. mutans 6715, less activity with RR g and low activity to LTA and dextran when tested by ELISA. Adsorption of this antiserum with whole cells of S. pyogenes resulted in antibody activity with specificity only to the serotype carbohydrate. The specificity of the antibody for homologous coating antigen was RR g greater than cell wall greater than whole cells. An antiserum to S. mutans MT573 (serotype e) contained antibody predominantly to LTA, whereas, anti-S. mutans MT703 (serotype e) reacted with both dextran and LTA; however, the activity to LTA was removed by prior adsorption of the antiserum with S. pyogenes cells. This treatment did not alter the antibody activity to dextran. To establish the sensitivity of ELISA, a purified IgG anti-serotype carbohydrate antibody was prepared by adsorption of anti-S. mutans 6715 antiserum with a mutant of S. mutans which lacks serotype carbohydrate followed by adsorption and elution of specific antibodies from S. mutans 6715 whole cells. The minimum level of sensitivity of ELISA was 12.5 ng of IgG anti-serotype carbohydrate.

Antibodies, Bacterial↗

Oral adjuvants enhance IgA responses to Streptococcus mutans.

The induction of immune responses to orally-administered trinitrophenyl (TNP)-haptenated Streptococcus mutans or its cell wall components and enhancement of immune responses with oral adjuvants has been studied in high IgA responsive C3H/HeJ mice and in gnotobiotic rats. Gastric intubation of TNP-S. mutans to LPS non-responsive C3H/HeJ or syngeneic, LPS responsive C3H/HeN mice induced IgA responses as determined by measuring splenic plaque-forming cell (PFC) responses and IgA anti-TNP antibodies in serum, saliva, and urine. Higher IgA responses always occurred in C3H/HeJ mice given oral S. mutans antigen than similarly treated C3H/HeN animals. Oral administration of the adjuvants concanavalin A or S. mutans cell wall peptidoglycan (PG) with antigen resulted in augmented IgA responses, especially in C3H/HeJ mice. On the other hand, oral administration of muramyl dipeptide (MDP) with antigen boosted anti-TNP responses in C3H/HeN, but not in C3H/HeJ, mice. Gnotobiotic rats given S. mutans whole cells (WC) or purified cell walls (CW) by the oral route exhibited a salivary IgA immune response which was potentiated greater than twofold when antigen was given with PG or MDP. In other studies, S. mutans WC or CW antigen in water-oil-water (W/O/W) emulsion or liposomes was administered by gastric intubation to rats. Significant salivary IgA responses were induced with these antigen-adjuvant preparations. Although rats given S. mutans WC or CW were protected from S. mutans challenge, the greatest degree of caries immunity was obtained in animals which received antigen and adjuvant and which exhibited significant salivary IgA antibody levels. In preliminary studies, it was observed that local injection of rats in the salivary gland region with a ribosomal preparation from S. mutans resulted in a significant salivary IgA response and caries immunity. The potential for soluble and lipid carrier adjuvants in oral vaccines for induction of protective antibodies to S. mutans is discussed.

Acetylmuramyl-Alanyl-Isoglutamine↗