Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Relationship between depression of early protection against influenza virus infection and the decrease in the number of peripheral polymorphonuclear leukocytes in cyclophosphamide-treated mice was investigated using protein-bound polysaccharide (PSK), which had been shown to exert a potent restorative effect on leukocytopenia in immunocompromised hosts. Following intranasal inoculation with influenza virus (1.5 x 10(3) PFU) into untreated mice, the pulmonary virus titer progressively increased during 3 days and decreased gradually from the day 7 after infection. The treatment of mice with cyclophosphamide (150 mg/kg) 2 days before infection markedly enhanced the pulmonary virus multiplication from the early phase of infection, and the higher virus titer was maintained thereafter. When mice were given cyclophosphamide after PSK-treatment, virus titers from the early to late phases of infection were lower than those in untreated mice.
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PMID:Depression of early protection against influenza virus infection by cyclophosphamide and its restoration by protein-bound polysaccharide. 133 97

Effector mechanisms responsible for resistance against ectromelia virus including antiviral activity of non-immune macrophages, antiviral antibody, delayed footpad reaction to viral antigen, and interferon induction after viral infection were depressed in BALB/c mice bearing syngeneic Meth A tumor. The degree of viral growth correlated well with the depression of delayed footpad reaction, antibody production, and interferon induction. Therefore, modification of macrophage functions by a tumor-bearing state and treatment with PSK may contribute to this modification of antiviral resistance, at an early phase of infection. Cytotoxic activity may not be the principal effector, since the cytotoxicity was induced in normal and tumor-bearing mice to almost the same extent yet an extensive viral growth occurred only in the latter.
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PMID:Depression of protective mechanism during the early phase of a viral infection in tumor-bearing mice and prevention by PSK. 242 96

C3H/He mice were inoculated with Pseudomonas aeruginosa by various routes 1 day after X5563 transplantation or 4 days after cyclophosphamide (CY) administration. Administration of PSK (Krestin) i.p. or p.o. to the tumor-bearing mice or CY-treated tumor-bearing mice resulted in an increase in survival rates. Viable P. aeruginosa were inoculated i.v. on day 0 into mice inoculated with tumor cells on day -12 and vaccinated with killed P. aeruginosa on day -10, or into mice inoculated with tumor cells on day -15, treated with CY on day -14 and vaccinated on day -10. Resistance to infection, which is enhanced by vaccination, was depressed by tumor burden or treatment with CY, but such depression was prevented by PSK administration.
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PMID:Influence of PSK (Krestin) on resistance to infection of Pseudomonas aeruginosa in tumor-bearing mice. 311 42

PSK (Krestin) is a protein-bound polysaccharide isolated from cultured mycelia of Coriolus versicolor in basidiomycetes. PSK is a biological response modifier which possesses unique characteristics. We investigated the effects of PSK on the immune response of aged C57BL/6 mice bearing a syngeneic transplantable tumor adenocarcinoma 755. (a) In C57BL/6 mice, the delayed foot pad reaction against sheep erythrocytes and resistance to syngeneic tumor challenge reached a peak when the mice were at 30 weeks of age, and decreased at 50-60 weeks of age. The serum of normal mice exerts a modifying effect on blastogenesis of lymphocytes to phytohemagglutinin. The positive effect reached a peak at 30 weeks of age, and thereafter declined with age. (b) When adenocarcinoma 755 was inoculated to C57BL/6 mice at 10-, 30- and 60-weeks of age, immune responses were depressed in 10-week-old and 60-week-old mice. PSK prevented such depression. However, in 30-week-old mice, tumor-induced suppression was slight, and administration of PSK to them increased proportion of mice which did not develop a tumor. (c) In 60-week-old tumor-bearing mice, the antitumor effects was increased with a combination of PSK and adoptive transfer of spleen cells from 10-week-old normal mice. The immune responses of mice, which change with the progress of age, are depressed by tumor burden. The administration of PSK to aged mice is effective to restore immune responses from tumor-induced suppression.
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PMID:Restoration of immune responsiveness by a biological response modifier, PSK, in aged mice bearing syngeneic transplantable tumor. 343 May 62

PSK is a protein-bound polysaccharide prepared from cultured mycelium of Coriolus versicolor. The effects of PSK on immunologic responsiveness were investigated in C3H/He mice bearing syngeneic X5563 tumor. The results were as follows. elayed foot pad reaction and antibody-forming capacity to sheep erythrocytes were depressed in tumor bearing mice, and such depression was prevented by oral or intraperitoneal administration of PSK. In vitro cytotoxic activity of splenic lymphocytes against the tumor was augmented by PSK administration. Antitumor effect was augmented by combination of PSK and X-irradiation. Delayed foot pad reaction to sheep erythrocytes was suppressed in normal C3H/He mice given immunosuppressive substance obtained from tumor-bearing mice, and the depressed reaction recovered to the normal level following PSK administration. These results show that PSK is effective in the syngeneic murine tumor system.
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PMID:[Restoration of depressed immune responses by PSK in C3H/He mice bearing the syngeneic X5563 tumor]. 378 56

Effector mechanisms responsible for protection against ectromelia virus (EMV) including antiviral activity of non-immune macrophages, cytotoxic T cells, antiviral antibody, delayed footpad reaction to viral antigen and interferon induction after viral infection were depressed in BALB/c mice bearing syngeneic Meth A tumors. The degree of viral growth correlated well with the depression of delayed footpad reaction, antibody production and interferon induction. But a control level of these elements could be obtained by pretreatment of tumor-bearing mice, with PSK Cytotoxic activity may not be the principal effector, since cytotoxicity was induced in both normal and tumor-bearing mice to almost the same extent but an explosive viral growth was observed only in the latter. These results suggest that PSK was responsible for restoring the depressed antiviral protective immunity to normal levels in tumor-bearing animals.
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PMID:[Depression of protective mechanisms against ectromelia virus infection in tumor-bearing mice and its prevention by PSK]. 609 65

The effect of PSK on the depressed bactericidal activity of macrophages and delayed-type hypersensitivity (DTH) to Listeria monocytogenes in BALB/c mice bearing transplantable Meth A fibrosarcoma was studied. In tumor-bearing mice pretreated with PSK, L. monocytogenes was cleared rapidly from the circulating blood and bacterial growth in the liver was inhibited effectively in the early phase of infection. This resistance to the infection could be transferred with peritoneal exudate cells (PEC) but not with non-adherent PE cells of PSK-treated mice. In the early phase of infection, tumor-bearing mice developed a lower level of DTH to L. monocytogenes than did nongrafted control mice. However, the control levels of DTH could be obtained by pretreatment of tumor-bearing mice with PSK. These results suggest that the restoration of resistance to L. monocytogenes in tumor-bearing mice by PSK may be ascribed to both prevention of depression or activation of macrophage function and prevention of depression of T cell-mediated immunity.
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PMID:[Effect of PSK on the recovery of macrophage function and T cell-mediated immunity in tumor-bearing mice]. 633 49

It was clear that the proportion of high mobility cells in thymus tended to increase during tumor development by cell electrophoresis. Although the antitumor activity of PSK, protein-bound polysaccharide or mitomycin-C was similarly effective in sarcoma-180-bearing mice, the histogram pattern of thymocyte electrophoresis differed markedly from each other. Normally, the proportion of high mobility cells of thymocyte increased more with the administration of mitomycin-C than that of the untreated tumor-bearers, while PSK kept the thymic cell mobility histogram normal. Changes of thymocyte electrophoresis caused by the drugs also correlated with the depression of their antiinfectious activity. Using the fully automated cell electrophoretic instrument, the drug can be evaluated simply from the viewpoint of antiinfectious efficacy.
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PMID:Evaluation of PSK, an antitumor protein-bound polysaccharides, by thymocyte electrophoresis. 644 39

Cell-mediated systemic immunity and immuno-reactivity of the regional lymph node in patients with gastric cancer were investigated. The studies were undertaken on the parameters such as skin test (PHA, PPD, Candida and SK-SD), T-cell subpopulation and lymphocyte blast formation . And concerning the regional lymph node, percentage of T-cell and blast formation were examined. The following results were obtained. There were correlations between the nonspecific parameters (PHA skin test, count of active T-cell and PHA blast formation ) and the staging according to the Japanese Research Society for Gastric Cancer. There were also correlations between the stage and the percentage of T-cell, PHA blast formation with and without autoserum in the immunity of the proximal regional lymph node. Correlations between the PHA blast formation in the proximal lymph node and the nonspecific parameters such as PHA, Candida skin test, count of the active T-cell and PHA blast formation in the peripheral lymphocyte were observed. The immunity of the distant regional lymph node was impaired in the patients of stage IV and III with 4 metastatic lymph nodes or more. Preoperative administration of PSK prevented impairment of cell-mediated immunity after operation. Patients administrated lentinan before operation got rid of depression of immunity in the proximal regional lymph node.
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PMID:[Nonspecific cell-mediated immunity in gastric cancer patients - with special reference to immuno-reactivity of the regional lymph node and preoperative immunotherapy]. 661 95

Immunopotentiators may mitigate the depression of immunological function caused by the cancer itself or by chemotherapeutics. However, it has been found that these immunopotentiators reduce the metabolic activity of the host against drugs, including "masked" chemotherapeutics, which might be activated by metabolization in the body. Reported here is the result of serial experiments carried out on the activation of cyclophosphamide (CPM) in tumor-bearing animals, pretreated with phenobarbital, a drug-metabolizing enzyme inducer, and coenzyme Q10, a physiological activator of the electron transfer system in mitochondrias, in combination with immunopotentiators. Female Donryu rats (120 g body weight) implanted with Yoshida Sarcoma cells (YS) (2.5 X 10(6) i.p.) were treated with CPM (160 mg/kg X 1 i.p.), 84 hrs after implantation; the levels of the normustard-like substances (active metabolites of CPM) were serially measured. Some of the animals were also treated with PSK (125 mg/kg X 5 i.p.), a proteinpolysaccharide immunopotentiator obtained from mycelia of the Coriolus vesicolor, or with OK-432 (10 KE/kg X 5 i.m.), a streptococcal immunopotentiator. The results obtained were as follows: The blood levels of the normustard-like substances were lowered, i.e. the CPM activation was depressed in the YS-bearing rats and the depression was markedly intensified by PSK or OK-432 administration. Phenobarbital (40 mg/kg X 3 i.p.) or coenzyme Q10 (5 mg/rat X 5 i.p.) administration could mitigate the depression of the blood levels caused by the immunopotentiators, and the combination of phenobarbital with coenzyme Q10 could recover the blood levels up to those of the YS-bearing control rats, or even higher. YS-implanted (i.p.) rats treated with CPM+ immunopotentiators+coenzyme Q10 survived longer than those treated with CPM+immunopotentiators. These findings suggest the usefulness of coenzyme Q10 for the enhancement of cancer immunochemotherapy using masked compounds combined with immunopotentiators; all the more so, because coenzyme Q10 has also an immuno-stimulating effect, moreover, it presents almost no side effects in clinical application.
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PMID:[Coenzyme Q10 in cancer chemotherapy--experimental studies on augmentation of the effects of masked compounds, especially in the combined chemotherapy with immunopotentiators]. 688 95


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