Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0153470 (Spleen)
 4,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of administration of PSK (Polysaccharide Kureha), a Coliolus preparation, in Meth-A solid tumors was analyzed in BALB/c mice. Spleen cells prepared from normal, non-treated Meth-A bearing, PSK-treated normal and PSK-treated tumor bearing mice were examined for induction of macrophage chemotatic factor (MCF). Only spleen cells from the latter mice produced MCF after 48 hrs of cultivation in the presence of Meth-A cells or concanavalin A (Con A). MCF-producing cells were indicated to be Lyt-1 positive, L3T4 positive and Lyt-2 negative cells in the negative elimination assay. There were no differences in the production of other cytokines including interleukin-2, interferon and tumor necrosing factor, spleen cells obtained other different groups of mice. The antitumor effect of either crude or purified MCF (molecular weight 100,000) was examined by daily consecutive intratumoral injections into Meth-A tumor tissues, and a significant inhibitory effect was detected.
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PMID:Antitumor effect of a Coliolus preparation, PSK: induction of macrophage chemotactic factor (MCF) in spleens of tumor bearing mice. 129 Jul 21

The antitumor effects of biological response modifiers (BRM) in a new experimental mouse model, the "double grafted tumor system", were analysed. BALB/c mice received simultaneous inoculations of Meth-A fibrosarcoma cells on right flank (10(6) cells) and left flank (2 x 10(5) cells) on day 0, and BRMs were injected intratumorally into right tumor on day 3, 4 and 5. The growth of the left-flank tumor was the real target for the evaluation of a given drug after 21 days. PSK (a protein-bound polysaccharide preparation), IL-1 and Cepharanthin cured not only the right, but also the left, non-treated tumor in a double grafted tumor system. OK-432 (a Streptococcus preparation) and BCG cured the right tumor and inhibited the growth of the left tumor. Lentinan (a polysaccharide preparation) inhibited neither the right nor the left tumor. Spleen cells from PSK-treated tumor bearing mice produced macrophage chemotactic factor (MCF) after 48 hrs cultivation in the presence of Con A or Meth-A tumor cells. MCF producing cells were indicated to be L3T4 positive cells. On the other hand, PMN activated by PSK treatment produced MCF in the culture supernatant. Therefore, our present and previous studies on the antitumor effect of BRM in the double grafted tumor system show that intratumoral administration of BRM first induces neurophils in the right tumor via an IL-8-like factor and then cytotoxic macrophages are induced by MCF. Then Lyt-1 (L3T4)-positive cells are induced in the right regional lymph nodes and in the spleen, probably via IL-1, which might be produced from macrophages in contact with tumor cells. Subsequently, Lyt-1-positive cells reach the left tumor through the blood stream, come into contact with Meth-A tumors and then produce MCF. Intratumoral administration of PSK in the right tumor thus induces cytotoxic macrophages in the left, non-treated tumor, thereby bringing about the regression of the distant tumor.
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PMID:[Differences of antitumor effect of various BRMs by intratumoral administration]. 153 Feb 88

The antitumor effect at a distant site of PSK, a Coriolus preparation, was analyzed with the double grafted tumor system in which BALB/c mice received simultaneous intradermal inoculations of Meth-A tumor in the right (10(6) cells) and left (2 x 10(5) cells) flanks and were then injected with PSK in the right-flank tumor on day 3. PSK inhibited the growth of not only the right but also the left (non-treated) tumor. Immunized spleen cells were taken from mice which had been cured by the intratumoral administration of 5 mg of PSK and were injected into the Meth-A tumor on day 3. Adoptive transfer of PSK immunized spleen cells caused the complete regression of Meth-A tumors. The effector cell activity was lost only after treatment with anti-Lyt-1 monoclonal antibody plus complement. Spleen cells and right and left regional lymph node cells prepared from PSK immunized mice were examined for Thy-1, Lyt-1, Lyt-2 and asialo GM1 phenotypes. The number of Lyt-1-positive lymphocytes increased in the right regional lymph nodes after intratumoral administration of PSK. A massive accumulation of macrophages and polymorphonuclear leukocytes was found in the right tumor and an infiltration of macrophages and Lyt-2-positive lymphocytes was found in the left (non-treated) tumor by immunohistochemical analyses. These results suggest that intratumoral administration of PSK induces Lyt-1-positive cells first in regional lymph nodes, then in the spleen, and subsequently induces macrophages and Lyt-2-positive cells in the left (non-treated) tumor, thus bringing about the regression of metastatic tumors.
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PMID:Antitumor effector mechanism at a distant site in the double grafted tumor system of PSK, a protein-bound polysaccharide preparation. 314 30

The antimetastatic effect of PSK was analysed with the "double grafted tumor system" in which BALB/c mice received simultaneous intradermal inoculations of Meth-A in the right (10(6) cells) and left (2 X 10(5) cells) flanks and were then injected with PSK in the right tumor on day 3. PSK inhibited the growth of not only the right but also the left, non-treated tumor. Immunized spleen cells were taken from mice which had been cured by the intratumoral administration of 5 mg of PSK. On day 3, one hour after intravenous injection of cyclophosphamide, immunized spleen cells (2 X 10(7) cells/mouse) were injected into the Meth-A tumor. Adoptive transfer of PSK immunized spleen cells caused the complete regression of Meth-A tumors. The effector cell activity was lost only after treatment with anti-Lyt-1 monoclonal antibody plus complement. Spleen cells and right and left regional (axillary and inguinal) lymph node cells prepared from PSK immunized mice 7 and 14 days after tumor inoculation were examined for Thy-1, Lyt-1, Lyt-2 and asialo GM1 phenotypes by flow cytometric analysis. The number of Lyt-1 positive lymphocytes increased in the right regional lymph nodes after intratumoral administration of PSK. Immunohistochemical analyses of the right and left tumors in the "double grafted tumor system" on day 7 and day 14 were carried out by PAP (peroxidase antiperoxidase) method. Necrosis, karyoklasis and a massive accumulation of macrophages were found in the right tumor after intratumoral administration of PSK. An infiltration of macrophages and Lyt-2 positive lymphocytes was found in the left, non-treated tumor. These results suggest that intratumoral administration of PSK might induce Lyt-1 positive cells first in regional lymph nodes, then in the spleen, and subsequently induce macrophages and Lyt-2 positive cells in the left, non-treated tumor of the "double grafted tumor system", thus bringing about the regression of metastatic tumors.
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PMID:[Antitumor effect of PSK (2): effector mechanism of the antimetastatic effect in the "double grafted tumor system"]. 359 18

Spleen and thymus cells from X5563 plasmacytoma-bearing mice treated with PSK (krestin) were analyzed by cell electrophoresis and flow microcytometry. A splenocyte electrophoretic pattern showed that an intermediate mobility peak (IMC), which appeared between the low (B cells) and high (T cells) peaks as the tumor developed, was depressed by the administration of PSK. Thy-1+ cells and asialo-GM1+ (aGM1+) cells decreased with tumor growth, and null cells without a marker of Ig, Thy-1 nor aGM1 increased. However, these changes were corrected by the administration of PSK. As the tumor grew, a thymocyte electrophoretic pattern showed that the incidence of low mobility cells, corresponding to immature cells, decreased, and that of high mobility cells, corresponding to mature cells in the medullary zone, increased. However, PSK suppressed the changes. The tumor did not disappear but life span was prolonged (121%) by the administration of PSK. These results lead to the conclusion that the administration of PSK prevented the changes in surface charge and markers of lymphocytes due to tumor burden, and restored the immunological responsiveness even in the syngeneic system.
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PMID:Effects of PSK, an antitumor protein-bound polysaccharide, on the surface charge of lymphocytes in X5563-bearing mice. 368 50

We previously reported that the extract of seeds from Aeginetia Indica L (AIL), a parasitic plant, induces potent antitumor immunity in tumor-bearing mice and that CD4+ T cells appear to be the main contributors in the induction of antitumor resistance. The present study was set up to investigate the in vitro effects of AIL on various lymphoid cells. Spleen cells from mice pretreated with AIL every 2 days for 1 week produced interleukin 2 (IL-2), interferon gamma (IFN gamma), tumor necrosis factor (TNF) and interleukin 6 (IL-6) when these cells were stimulated in vitro by AIL. Further, we found that CD4+ T cells were main producers of IL-2 and TNF upon the stimulation with ALL in vitro, while both CD4+ and CD8+ T cells secreted IFN. On the other hand, ALL was mitogenic in vitro to T enriched splenic lymphocytes as well as B enriched splenic lymphocytes. Moreover, AIL also proliferated thymocytes and this activity was potently synergistic with a suboptimal dose of concanavalin A (Con A). Lipopolysaccharide (LPS) contamination in AIL preparation was negligible since proliferative activity of AIL to B enriched splenic lymphocytes was not influenced in the presence of an endotoxin antagonist, polymyxin B sulfate (PMB). Further, B cell mitogenic activity of AIL seems to be mediated by different mechanism(s) from that of LPS since ALL could proliferate B enriched lymphocytes of C3H/HeJ mice which do not respond to the stimulation with LPS. A well known biological response modifier (BRM), Krestin (PSK), had no ability in inducing either T or B lymphocyte activation in vitro as shown by AIL.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Seed extract of Aeginetia indica L induces cytokine production and lymphocyte proliferation in vitro. 820 51