Biomedical subjects
Publications and source records attributed to T Kajikawa.
A case of hepatic encephalopathy due to portal hypertension with a rare porto-caval shunt was presented with special reference to MRI. Markedly dilated collaterals of pancreatico-duodenal vein and right ovarian vein were clearly revealed in MRI or PTP. MRI is useful and indispensable to evaluate various porto-systemic communications.
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Involvement of the Harderian gland (HG) in the production of lacrimal immunoglobulin (especially IgA) was investigated. The lacrimal concentration of each immunoglobulin class was not affected by surgical bursectomy but was reduced by cyclophosphamide (CY) and testosterone (TP) treatments. Surgical removal of the Harderian gland caused a remarkable reduction of both the lacrimal concentration of each immunoglobulin class and the specific antibody titre, and and IgA was almost undetectable. The lacrimal concentration of each immunoglobulin class, as well as the specific antibody titre, was not affected by surgical removal of the Lacrimal gland (LG). The route of antigen administration produced no difference in the class of lacrimal immunoglobulin produced. The results indicate that the production of immunoglobulin in chicken tears may be dependent on the HG and that lacrimal immunoglobulin may be synthesized and secreted locally in the HG. Lymphocytes of the HG are of bursa of Fabricius origin and are seeded into the HG prior to hatching and its lymphocytes do not appear to be involved in systemic immunity.
The ability of heterologous fibrinogen in combination with interferon (IFN)-gamma to induce endogenous production of cytotoxic factor was examined. Heterologous but not homologous fibrinogen induced high production of cytotoxic factor in IFN-gamma-primed mice. The cytotoxic activity was maximal 1 h after this triggering. The LD50 value of heterologous fibrinogen in mice was greater than 250 mg/kg i.v. But heterologous fibrinogen induced antibody, causing anaphylaxis. Therefore, the effect of successive injections of fibrinogens from a different species was tested. Cytotoxic factor could be produced repeatedly by successive treatments with a combination of IFN-gamma and heterologous fibrinogen from one species for 1 week, although the cytotoxic activity induced by successive injections gradually decreased. After the decrease of the triggering effect of heterologous fibrinogen of one species, heterologous fibrinogen from a different species could induce cytotoxic activity at the same level as that after the first triggering. Thus, a combination of IFN-gamma and heterologous fibrinogen is effective for cytotoxic factor production, provided different heterologous fibrinogens are used successively. This combination should be useful for endogenous cytotoxic factor production in clinical trials.
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The triggering activities of heterologous fibrinogen and fibrin on endogenous production of tumor necrosis factor (TNF)-like cytotoxic factor in vivo were examined. The triggering activities of fibrinogen or fibrin from four species injected into the peritoneal cavity of C3H/He mice infected i.p. with bacillus Calmette-Guérin (BCG) were tested. Heterologous, but not homologous, fibrinogen and fibrin showed triggering activity. The route of triggering by heterologous fibrinogen to elicit TNF-like activity systemically was studied. Injection of heterologous fibrinogen i.v. into mice infected i.v. with BCG resulted in a 40-fold higher serum TNF-like activity level than after its i.p. injection. The serum TNF-like activity level was maximal 1 h after i.v. injection of heterologous fibrinogen. When heterologous fibrinogen was injected several times i.v. into mice bearing solid-tumors, TNF-like activity was also released into the serum after every injection, although the activity decreased progressively on second and third injections to 10 and 1%, respectively, of that after the first injection. We used heterologous fibrinogens derived from different species for triggering every week to avoid this gradual decrease of TNF-like activity. In this way TNF-like activity was induced as highly as the primary induction. These results showed that TNF-like cytotoxic factor could be produced in vivo locally or systemically by heterologous fibrinogen or fibrin. Thus both agents should be useful as nontoxic triggering agents.
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Human lectin purified from placenta induced release of cytotoxin from a murine macrophage cell line and human peritoneal monocytes. This activity was not due to contamination of the lectin preparation with lipopolysaccharide.
The effects of interferons (IFNs) and interleukin 2 (IL 2) on endogenous production of tumor necrosis factor (TNF) were investigated in mice. Production of serum TNF was triggered by iv injection of OK-432 and tested by in vitro cytotoxicity assay. Injection of recombinant IFN-gamma with OK-432 and tested by in vitro cytotoxicity assay. Injection of recombinant IFN-gamma with OK-432 or of IFN-alpha/beta, recombinant IFN-beta, recombinant IFN-alpha A/D or recombinant IL 2 six hours before OK-432 enhanced TNF production about 10-fold, which indicated priming actions of these compounds in TNF production. These findings suggest that these compounds could also be used as priming agents for endogenous production of TNF in cancer patients.
The effect of tuberculin-antigen protein (PPD: purified protein derivatives) on the priming of tumor necrosis factor (TNF) a long time after sensitization with bacillus Calmette-Guérin (BCG) was investigated in mice. Mice were infected intravenously (i.v.) with 4 X 10(7) colony-forming units (CFU) of BCG per mouse, and the TNF activity triggered by 15 micrograms lipopolysaccharide (LPS) was assayed with time using L-929 cells. The activity was maximal 4 weeks after sensitization and decreased to the control level after 10 weeks. The i.v. injection of 10 micrograms of PPD per mouse enhanced the TNF production triggered by LPS in mice even 10-20 weeks after sensitization. This enhancement was unexpectedly quite transient, being maximal 3 h after PPD treatment. The activity was comparable to that in mice 4 weeks after sensitization of BCG (without PPD). The enhancing effect of PPD was observed in the dose range of 0.1-10 micrograms/mouse, and 10 micrograms of PPD significantly enhanced the TNF activity triggered by even 0.6 microgram LPS. These findings indicate that priming of sensitized animals with some antigens followed by triggering with LPS induces a significant endogenous production of TNF even a long time after antigen sensitization. The possible application of these findings for inducing endogenous production of TNF in human patients by use of tuberculin allergy is discussed.
In an attempt to find nontoxic triggering agents to release cytotoxin from primed macrophages of mice, the abilities of eight plasma components to induce release of cytotoxin from J-774.1, a murine macrophage-like cell line, were examined. Heterologous, but not homologous, fibrinogen and fibrin were found to enhance the release of cytotoxin. The fibrinogen and fibrin did not contain any lipopolysaccharide (LPS) as tested with polymyxin B. Thus, heterologous fibrinogen and fibrin could be useful as nontoxic triggering agents.
C3H/He mice were immunized i.v. with sheep red blood cells (SRBC), and then the effect of i.v. challenge with SRBC on the priming of endogenous production of tumor necrosis factor (TNF) was investigated. Mice were immunized i.v. with 10(8) SRBC/mouse, and their serum TNF activity, triggered by 3 micrograms lipopolysaccharide (LPS) per mouse, was assayed by an in vitro cytotoxicity test using L-929 cells. Anti-SRBC antibodies were induced maximally in 2 weeks, but the acquired immunity did not affect TNF triggering. However, 9-10 weeks after the primary challenge, when there was still a relatively high antibody titer in the serum, i.v. rechallenge with 10(8) SRBC/mouse transiently enhanced the TNF activity triggered by LPS to about 10 times that in normal control mice. This priming effect of SRBC challenge was antigen specific, because challenge with horse red blood cells (HRBC) had no effect. SRBC opsonized with anti-treated with anti-SRBC antiserum or sonicated SRBC had no effect. These findings suggest two ways of facilitating the triggering of endogenous TNF production: booster challenge of immunized animals with the corresponding antigens makes them ready for TNF triggering, and direct injection of immune complexes, even into normal animals, makes them ready for triggering of TNF. The possible application of these findings for inducing endogenous TNF production in human cancer patients by use of immune complexes is discussed.
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Explore the source record for details and available documents.
Explore the source record for details and available documents.