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Biomedical subjects

A Kojima

Publications and source records attributed to A Kojima.

At least 289 records · Page 16Linked to original sources
PubMed1981

Genetic susceptibility to post-thymectomy autoimmune diseases in mice.

The strain distribution pattern of five different post-thymectomy autoimmune diseases was determined in 21 inbred and two congenic, resistant strains of mice. The results indicated that susceptibility genes outside the H-2 complex may be involved in the development of localized autoimmune diseases in neonatally thymectomized mice. Studies of recombinant inbred strains also showed that susceptibility to gastritis was not associated with the H-2 haplotype but appeared to be influenced by a minor histocompatibility locus. Possible linkage to the H-2 complex was suggested only in the development of coagulating gland adenitis. Although one experiment showed that susceptibility to orchitis and coagulating gland adenitis was inherited as a recessive trait, further studies are required to determine the exact mode of inheritance in each disease system.

Animals↗
PubMed1981

Regulatory mechanism of delayed-type hypersensitivity in mice. III. In vitro analysis of memory T cells involved in augmentation of DTH responses.

The memory of delayed-type hypersensitivity (DTH), manifested by the augmented responsiveness upon challenge with alum-absorbed ovalbumin (OA), was induced in mice primed 7 days, 21 days, or 90 days previously with 1 microgram of reduced and alkylated OA. The memory cells involved in the augmentation of DTH responses were analyzed in the in vitro induction system of T cells which mediate DTH against OA. Spleen cells from the primed mice generated DTH-effector T cells (DTH-Te) in a significantly accelerated fashion, compared with unprimed spleen cells, when cultured with OA. The accelerated generation of DTH-Te in vitro was induced antigen specifically and was dependent on a certain T cell population in the primed spleen. The T cell population was found in the spleen of primed mice for at least 3 months after priming, corresponding to the persistence of DTH-memory in vivo. Moreover, it was fractionated in the high-density layer by discontinuous bovine serum albumin gradient centrifugation. The high-density cell population decreased in density with increase in the time of culture and developed into DTH-Te, which were separated in the low-density layer on day 4 of culture. These results indicate that the T cells involved in the accelerated generation of DTH-Te in vitro are long-lived DTH-memory T cells, which are probably precursor cells, capable of differentiating into DTH-Te upon challenge with the antigen.

Animals↗
PubMed1981

Correlation between production of inflammatory substances and generation of effector T cells mediating delayed-type hypersensitivity in mice.

In vitro exposure to human serum albumin (HSA) of splenic lymphocytes from mice sensitized for delayed-type hypersensitivity (DTH) against HSA resulted in the release of substances that could induce a footpad inflammatory reaction with a maximum of 6 hr after injection into normal mice. The substances were fractionated mainly in a molecular weight range of 30,000 to 70,000 daltons on Sephadex G-200. The ability of sensitized lymphocytes to produce the substances was dependent on T cells, was antigen specific, and correlated well with the ability of the lymphocytes to mediate DTH reactions. Moreover, the substances were produced efficiently by the DTH effector cell population generated in the in vitro culture system and also by the effector cell-enriched fractions on discontinuous bovine serum albumin gradients. These results suggest that the substances are produced by DTH-effector cells.

Animals↗
PubMed1981

[Canine parvovirus infection in a group of beagles (author's transl)].

An outbreak of canine parvovirus infection in a group of 26 beagles was described. The disease characterized by acute intestinal involvement was highly contagious but fatality was low (1/26). Transient leukopenia was recorded in some animals. All the convalescent sera were positive in agar gel diffusion test using feline panleukopenia virus antigen. Histopathological examination on fetal dog revealed regressive change associated with formation of amphophilic intranuclear inclusion bodies in the enterocytes of the Lieberkühn's crypt and regressive change in the lymphoid tissues. Pathologic picture exhibited strikingly resemblance with that of feline panleukopenia.

Animals↗
PubMed1981

Acute effects of cadmium on delayed-type hypersensitivity in mice.

A single exposure of mice to cadmium resulted in suppression of the induction of primary delayed-type hypersensitivity (DTH) responses as well as memory T-cell and suppressor T-cell activities, augmenting and inhibiting DTH respectively. Furthermore, cadmium suppressed the expression of already established DTH, in immune mice, even though DTH-effector T cells in the spleen of immune mice were not affected by cadmium injection. Such suppressive effects were demonstrated when cadmium was administered within 2 days before immunization or elicitation for DTH. Cadmium caused also within 2 days in mice thymic involution and splenomegaly. These results indicate that cadmium inhibits not only the generation of certain populations of T lymphocytes for DTH but also some mechanisms in the host involved in the expression of DTH.

Animals↗
PubMed1981

Experimental production of pulmonary granulomas. I. Immune granulomas induced by chemically modified cell walls and their constituents.

The intrabronchial instillation of stimulants in an oily vehicle induces a solitary inflammatory focus in the rabbit lung. When heat-killed tubercle bacilli were administered to tuberculo-immune animals, a necrotizing focus with cavities was induced. Delipidation of the bacterial cells stimulated the production of a necrotizing focus. In contrast, acetylation of the mycobacterial cell walls resulted in the replacement of cavity formation with epithelioid-cell granuloma production similar to that seen after the administration of Wax D, a peptidoglycolipid fraction of the cell walls. These lesions were induced much faster than in controls, indicating that some immune mechanisms are involved. In the present study of the specific granuloma induction mechanism, the biological activities of the chemical constituents of Wax D were examined. It was concluded that specific granuloma induction is due to the long delayed hypersensitivity antigenicity of Wax D which is brought about by the conjugation of biologically inactive mycolic acid with Arthus-antigenic peptidoglycan. Wax D glycolipids with delayed-type antigenicity also take part in the induction. The intrinsic adjuvant activity of these compounds may stimulate granuloma production. The haemagglutination antigenicity and Arthus-type antigenicity of the polysaccharide or peptidoglycan moiety are not involved.

Acetylmuramyl-Alanyl-Isoglutamine↗
PubMed1981

Fine structure of giant hypertrophic gastritis developed in thymectomized mice.

(C3H/HeMs x 129/J)F1 mice were thymectomized at 3 days of age, and their stomachs were examined by electron microscopy at 3, 6, and 18 months of age. A hypertrophic type of gastritis developed in about half the mice, the fundus being chiefly affected. In the early stage, thickening of the mucosa was attributed mainly to an elongation of the glandular part, but in the later stage it was attributed to both elongated glandular tubules and proliferated foveolar cells. Mature parietal and chief cells were preferentially reduced in number, and immature counterparts were relatively marked in the glandular portion. Thus, the proportion and grade of maturation of these cells in gastritic mice were different from those in normal mice. Foveolar and glandular mucous cells, resembling, respectively, normal surface mucus and mucous neck cells, were the major cell types of the glands. Undifferentiated cells were also frequently encountered. Hyperplasia of endocrine cells, particularly ECL and G cells in the fundic and pyloric mucosa, respectively, was also documented. These results suggest that the gastric hypertrophy of gastritic mice was triggered by the disturbances in differentiation and maturation of parietal and chief cells.

Animals↗
PubMed1980

The suppressive effect of hepatic 9,000 x G supernatant fraction from 3-methylcholanthrene-treated rats on the mutagenic activity of 2-acetylaminofluorene.

Hepatic 9,000 x g supernatant (S9) fraction from 3-methylcholanthrene (MC)-treated rats showed a significantly low activity in the in vitro conversion of 2-acetylaminofluorene (AAF) to mutagen(s), while S9 fraction from untreated or phenobarbital (PB)-treated rats showed a remarkable activity. The S9 fraction from MC-treated rats actually suppressed the PB-S9 mediated AAF mutagenicity. Since the suppressive effect of MC-S9 was lost by the addition of 10(-4) M alpha-naphthoflavone (alpha-NF), rat specific cytochrome P-448 may be responsible for this suppressive effect.

2-Acetylaminofluorene↗
PubMed1980

Isolation and properties of sialodacryoadenitis virus of rats.

Pathogenic agents were isolated from affected salivary glands of rats with sialodacryoadenitis (SDA) by means of intercerebral inoculation to newborn mice and inoculation to primary rat kidney cell cultures. The properties of these isolates, irrespective of the isolation techniques, were in general agreement with that of SDA virus strain 681, and they were identified as SDA virus. In addition to the known properties, following characteristics were noticed: (1) Particles of SDA virus bore two different long and short surface projections. (2) Some antigenic differences were observed between the present isolate 930-10 and the strain 681. (3) It was suggested that SDA virus grew better at 35 degrees C than at 31 degrees, 33 degrees, 37 degrees or 39 degrees C. (4) SDA virus did not propagate in DBT cells.

Animals↗
PubMed1980

Pathological observations on natural cases of sialodacryoadenitis of rats.

Pathological observations were carried out on 100 male rats of Sprague-Dawley strain obtained from 5 outbreaks of sialodacryoadenitis (SDA). In accordance with clinical and macroscopic findings, principal microscopic changes were found in the salivary (submaxillary and parotid) and Harderian glands. Lesions observed in these different glands were essentially similar to each other, and characterized by degenerative changes in the epithelial cells of the ducts and acini associated with marked and extensive serous inflammation in the interstice. Furthermore, squamous metaplasia of the ductal epithelia was a common feature to these glands in the late stage of the disease. Some differences, however, were detected between the changes of the salivary glands and those of the Harderian glands. Firstly, the ductal epithelial cells were affected at first and the acinous epithelial cells were damaged only secondarily in the active inflammatory process in the salivary glands, while both ductal and acinous epithelial cells were involved equally in the primary lesion in the Harderian glands. Secondly, the increase in connective tissue elements in the reparatory process was extremely marked in the Harderian glands as compared with the salivary glands. Consequently, in the lesion of Harderian glands in the late stage, original construction was almost indiscernible, and the ducts and acini were only recognized as disseminated islets in actively proliferated connective tissue elements.

Animals↗
PubMed1980

Autoimmune oophoritis in thymectomized mice: detection of circulating antibodies against oocytes.

Previous studies from our laboratory described a particular type of ovarian dysgenesis which develops in mice after neonatal thymectomy (Tx) at the critical age of 2-4 days after birth. The present experiment provides evidence which strongly suggests an autoimmune aetiology for this phenomenon. By indirect immunofluorescence (IFL) and horse-radish peroxidase (HRPO) labelled antibody techniques, it was demonstrated that neonatally Tx mice of (C57B1/6Cr x A/JCr)F1 (B6A) and (C3H/HeMs x 129/J)F1 (C31) hybrids produce circulating autoantibody(ies) against ooplasma of oocytes (AOA) in growing follicles, but not against oocytes in primordial follicles. Appearance of AOA was closely correlated with the development of oophoritis which ws characterized by a rapid and complete loss of oocytes at early adulthood. In B6A and C31 mice, oophoritis occurred and AOA appeared in sera after Tx at day 3(Tx -- 3) but not after Tx at days 0 or 7. Also, in athymic B6A and C31 nude mice neither oophoritis or AOA were detectable. Complete absorption of AOA with homogenates of isogeneic normal adult ovaries, but not with homogenates of X-ray-irradiated anovular ovaries or granulosa cell tumour may indicate the specificity of AOA. AOA was first demonstrated at day 30-40 in sera of Tx mice, whose ovaries showed a marked enhancement of follicular degeneration and the death of numerous occytes with or without lymphocyte infiltration. High titres of AOA, detectable in sera of more than 2,000-fold dilutions, were assayed by the IFL technique at day 50-90; however, AOA gradually diminished in titre with age and disappeared at day 150-360 when no oocytes remained in the atrophic ovary. Mice thymectomized at day 3 occasionally produced autoantibodies against zona pellucida and with lesser frequency against steroid-producing cells of the ovary. These data indicate that in the mouse Tx at the critical age shortly after birth produces autoimmune oophoritis, subsequently resulting in early sterility.

Age Factors↗
PubMed1980

Experimental production of possible autoimmune castritis followed by macrocytic anemia in athymic nude mice.

A specific gastritis was induced in BALC/c (+/?) mice by thymectomy within 3 days after birth (25 to 45 per cent) or in BALB/c (nu/nu) mice by the injection of spleen cells (10(7)) from neonatally thymectomized mice (70 per cent). Normal peripheral lymphoid cells, irrespective of the sex and dose, were generally ineffective in inducing gastritis in nude mice, while thymus cells were partially effective (30 per cent). The induced gastritis was characterized by a loss of chief and parietal cells and by varying degrees of lymphoid cell infiltration along thickened muscularis mucosa. The fundic mucosa was replaced by mucous necklike immature cells, and there was a rise of pH of the gastric juice. Argyrophilic endocrine cells escaped the inflammation and increased in number. The gastritis induced in nude mice was generally more severe and was often followed by severe macrocytic anemia. Megaloblast-like large immature erythroid cells were numerous in the spleens of affected mice. Antiparietal cell antibodies (IgG) were always demonstrated by an indirect immunofluorescence test in the sera of gastritis-developing mice, but were absent in sera of normal or untreated conventional nude mice. These findings suggest a new animal model of pernicious anemia in man.

Anemia, Macrocytic↗