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Biomedical subjects

K Shoji

Publications and source records attributed to K Shoji.

At least 91 records · Page 5Linked to original sources
PubMed1988

In vitro increase of histidine decarboxylase activity and release of histamine by peritoneal resident cells of mast cell-deficient W/Wv mice; possible involvement of macrophages.

When peritoneal resident cells (PRCs) of genetically mast cell-deficient WBB6F1-W/Wv mice were cultured in vitro for 5 h at 37 degrees C, their histidine decarboxylase [HDC, L-histidine carboxylase, E.C. 4.1.1.22] activity increased 10-fold. Since inhibitors for energy production and mRNA and protein syntheses inhibited this increase of HDC activity, it appeared to represent de novo synthesis of the enzyme, i.e., induction. This increase was followed by an increase in the amount of histamine in the culture medium of the cells, indicating that histamine synthesized by the induced HDC was not stored in the cells but was quickly released. Mast cells were not involved in the HDC induction, because the extents of HDC induction in PRCs of W/Wv and wild type +/+ mice were similar. The removal of T cells with anti-Thy-1,2 antibody and complement from the PRCs did not affect the HDC induction, but the removal of phagocytes decreased the induction to one-tenth in spite of a 2-fold increase in the proportion of B cells in the PRCs. After separation of the PRCs into adherent and non-adherent fractions, the increase in HDC activity was found to be associated with the adherent fraction that was mostly positive to esterase staining. These results suggest that HDC was induced in peritoneal macrophages.

Animals↗
PubMed1988

New suppressor mutation sur0B of spo0B and spo0F mutations in Bacillus subtilis.

Two extragenic suppressor mutations, sur0B20 and sur0F1, which restore the sporulation of spo0B or spo0F mutants of Bacillus subtilis to the wild-type level, were obtained. These suppressor mutations were located in the spo0A gene. Their location is close to that of the sof-1 mutation, which suppresses spo0B, spo0E and spo0F mutations. However, spo0 strains bearing the sur0B20 mutation differed in several phenotypic characteristics from spo0 mutants bearing the sof-1 suppressor. Nucleotide sequence analysis revealed that the sur0B20 and sur0F1 mutations resulted in Glu14 to Val and Asn12 to Lys conversion, respectively, in the spo0A gene. This result indicates that sur0B20 is a new suppressor of spo0b and spo0F mutations, whereas sur0F1 is identical to sof-1.

Alleles↗
PubMed1987

Induction of histidine decarboxylase in non-mast cells in the spleen of mice by injection of staphylococcal enterotoxin A.

Injection of Staphylococcal enterotoxin A (SEA) into WBB6F1-W/WV mice genetically deficient in mast cells resulted in a 10-fold increase in the histidine decarboxylase [HDC, L-histidine carboxylase, EC 4.1.1.22] activity of their spleen. The nature of the spleen cells responsible for this increased HDC activity was studied. The HDC induction by SEA was abolished on day 1 after X-ray irradiation of the mice at 400 rad and restored by transplantation of bone marrow cells from normal WBB6F1-+/+ littermates into the X-ray irradiated WBB6F1-W/WV mice. Transplantation of cells from other organs of the normal mice, such as the thymus, mesenteric lymph node and spleen, did not restore the HDC increase significantly. Transplantation of cultured mast cells also did not restore the increase. Moreover, the high HDC activity of spleen cells induced by SEA was not affected by their treatment with anti-Thy-1,2 antibody and complement. Depletion of phagocytes from the spleen by treatment with carbonyl iron resulted in decrease in HDC activity. These results suggested that phagocytic cells derived from haemopoietic stem cells of the bone marrow were responsible for the increase in HDC activity induced by SEA.

Animals↗
PubMed1987

Induction of murine gamma interferon production by lipopolysaccharide and interleukin-2 in Propionibacterium acnes-induced peritoneal exudate cells.

Lipopolysaccharide (LPS) induces high levels of gamma interferon (IFN-gamma) in the circulation of mice pretreated with heat-killed Propionibacterium acnes. The following results were obtained in the present study. LPS, as well as interleukin-2 (IL-2), was also able to induce IFN-gamma in vitro in peritoneal exudate cells (PEC) from such mice. Splenocytes and lymph node cells from these mice or resident peritoneal cells from control mice produced trace or undetectable amount of IFN-gamma upon exposure to LPS. A synergistic effect on IFN-gamma induction was observed when LPS was added to a culture of PEC together with IL-2. Indomethacin augmented the induction of IFN-gamma by LPS or IL-2, and prostaglandin E2 reversed its effect. Deprivation of plastic-adherent or nylon wool-adherent cells abolished the induction by LPS or IL-2, whereas it did not affect that by concanavalin A. Culture supernatant of plastic-adherent cells incubated with LPS stimulated the nylon wool-nonadherent cells to produce IFN-gamma in the presence of IL-2, but interleukin-1 or phorbol myristic acetate did not replace the LPS-stimulated supernatant. The ability of PEC to produce IFN-gamma measured as a function of time after P. acnes injection increased in proportion to their natural killer (NK)-like activity against YAC-1 cells. Moreover, treatment of PEC with monoclonal anti-Thy-1 antibody or with anti-asialo GM1 antiserum plus complement eliminated the production of IFN-gamma and the NK-like activity simultaneously, whereas treatment with monoclonal anti-Lyt-2 antibody plus complement did not. These results suggest that IL-2 and some unidentified factor released from plastic-adherent cells by LPS stimulation cooperatively induce IFN-gamma production in activated, Thy-1- and asialo GM1-positive NK-like cells appearing in inflammatory reactions and that prostaglandin E2 regulates IFN-gamma production in these cells.

Animals↗
PubMed1985

Induction of histidine decarboxylase activity in the spleen of mice treated with staphylococcal enterotoxin A and demonstration of its non-mast cell origin.

Histidine decarboxylase (HDC) activity increased 13-, 7-, and 2-fold in the spleen, lung and liver, respectively, but not in other tissues of C57BL/6 mice injected i.v. with 50 micrograms/kg of Staphylococcal enterotoxin A (SEA). But even in the spleen, increase in the histamine level was only 1.5 times that of untreated mice. In genetically mast cell-deficient WBB6F1 - W/Wv mice HDC activity in the spleen increased to the same extent as in wild type WBB6F1 - +/+ mice on SEA treatment, but the histamine level in the spleen also increased 20-fold, whereas it increased only 1.4-fold in +/+ mice. These results suggest that the increases in HDC and histamine resulted from interaction of SEA with non-mast cells in tissues.

Animals↗
PubMed1985

Immunomodulating activities of staphylococcal enterotoxins. I. Effects on in vivo antibody responses and contact sensitivity reaction.

The immunomodulating effects of staphylococcal enterotoxins on in vivo immune responses in C57BL/6 mice were examined. Of the five serological types A (SEA), B, C, D, and E (SEE), only SEA and SEE markedly suppressed the antibody response to sheep red blood cells (SRBC) when injected 1 day before or on the day of immunization with SRBC. Further study of SEA revealed that it did not affect the antibody response to a thymus-independent antigen, salmonella flagella, but did affect the T-cell-mediated immune response. Contact sensitivity to dinitrofluorobenzene (DNFB) was suppressed when SEA was injected before sensitization or before challenge with DNFB, indicating that SEA affected both the afferent and efferent phases of DNFB contact sensitivity. As the suppression of DNFB contact sensitivity could be transferred by anti-Thy-1.2 antibody-sensitive spleen cells of SEA injected donors into normal or DNFB-sensitized recipients, the suppression was thought to be an active one. However, SEA could augment the DNFB contact sensitivity when injected on the third day after sensitization with DNFB. These results indicate that the immunomodulating effects of SEA can be mediated by the T-cell function.

Animals↗