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

Improved tolerance of splenectomized patients with Hodgkin's disease (HD) to radiotherapy and chemotherapy has been reported. The present study was undertaken to determine the effects of splenectomy and nitrogen mustard (NM) on colony-forming cells (CFC's) of bone marrow cells obtained from CF1 male mice by in bitro agar-gel technique. Splenectomized mice were given NM intraperitoneally on day 11. On day 15, they were sacrificed and the bone marrow was cultured with a source of colony-stimulating factor (CSF). Spleen extract was prepared by grinding spleens from CF1 mice. On the eighth day of incubation, significantly higher numbers of CFC's were found in splenectomized animals at 1% confidence level (F Test) compared with the nonsplenectomized animals. Both splenectomized and non-splenectomized mice had a greater colony response after NM (at 5% confidence level) than saline-treated controls. Maximum numbers of colonies were obtained in the nustard-treated asplenic animals. Splenic extract, as well as extracts from other organs, when added to the culture plates resulted in inhibition of colony formation. The significance of in vitro inhibition after addition of organ extract is uncertain.
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PMID:Effects of nitrogen mustard and splenectomy on mouse bone marrow colony formation in vitro. 95 68

The effects of lectins in the diet have been mainly studied in rats. An important question is whether results obtained in rats can be extrapolated to larger animals like the pig. Phaseolus vulgaris beans are rich in toxic lectins. Therefore a study was carried out to compare the effects of diets containing 200 g Phaseolus vulgaris beans (raw or toasted)/kg in rats and piglets. Live-weight gain, nitrogen digestibility and N balance were much lower in piglets than in rats fed on diets containing raw beans. Live-weight gain and N balance were slightly negative in the piglets. When toasted beans were given, live-weight gain and N balance values were reduced in piglets but hardly at all in rats. Giving raw beans caused hypertrophy of the pancreas in the rats but in piglets the weight of the pancreas was reduced. Spleen weight was depressed in the piglets but not in the rats. Weight of liver was not affected in either animal species. When toasted beans were given no effects on the weights of pancreas, spleen or liver were found in piglets or rats. It was concluded that the piglet is much more sensitive to antinutritional factors in the Phaseolus vulgaris bean than the rat.
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PMID:Comparison of growth, nitrogen metabolism and organ weights in piglets and rats fed on diets containing Phaseolus vulgaris beans. 226 82

The effect of acute exposure to nitrogen dioxide (NO2) on splenic T lymphocyte subpopulations was studied in C57BL/6cum mice. The mice were exposed to 4 ppm NO2 for 8 hr. Monoclonal antibodies to T lymphocyte differentiation antigens and fluorescence-activated cell sorter (FACS) analysis were used to detect changes in T lymphocyte subpopulations. Percentages of total T lymphocytes (Thy-1.2-positive), T-helper/inducer lymphocytes (L3T4-positive), and T-cytotoxic/suppressor lymphocytes (Lyt-2-positive) were significantly lower in NO2-exposed animals than in filtered-air-breathing controls. Large T-cytotoxic/suppressor cells were found to be the most susceptible subpopulation. Spleen and body weights of the mice were also determined. There were no differences between body weights of control and exposed animals; however, exposed mice had significantly lower spleen weights. This is the first report providing evidence linking alterations in T lymphocyte subpopulations to acute NO2 exposure at occupational levels. T lymphocytes play a central role in regulatory and effector immunological functions such as mediating delayed hypersensitivity, regulating immunoglobulin production, and lysing virus-infected and neoplastic cells. The biological significance of these findings remains to be established, but it is very likely that functional impairment occurs since an optimal immune response depends upon a proper balance of the T lymphocyte subpopulations. Detection of alterations in T lymphocyte subpopulations using monoclonal antibodies and FACS analysis may provide an extremely sensitive means of demonstrating NO2-induced changes in the immune system.
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PMID:Reduction in T lymphocyte subpopulations following acute exposure to 4 ppm nitrogen dioxide. 266 21

Lewis rats undergo a relapsing paralytic disease upon challenge with spinal cord emulsified in complete Freund's adjuvant (CFA). Treatment with two intracardiac injections of liposomes composed of whole myelin significantly reduced the severity of disease. Protection was disease-specific since treatment with myelin liposomes did not protect Lewis rats against adjuvant arthritis (AA), a CNS-unrelated T-cell-mediated autoimmune disease. Myelin-liposome-treated, spinal cord/CFA-immunized rats displayed borderline reduction of delayed-type hypersensitivity (DTH) (ear swelling) reactions to myelin and myelin basic protein (MBP), but significantly reduced in vitro lymphnode cell proliferation in response to these antigens. Responses to purified protein derivative of Mycobacterium tuberculosis (PPD) were not reduced, emphasizing the antigen-specific nature of the myelin-liposome-mediated suppression. Spleen cell proliferative responses were inconsistent and often poor. However, when cultured in the presence of NG-monomethyl-L-arginine (MMA), antigen-specific proliferation of spleen cells from both treated and control rats was greatly enhanced, indicating that reactive nitrogen intermediates contributed to the decrease in spleen cell proliferation. Purified splenic T cells from treated rats displayed a pattern of proliferation similar to that of unseparated lymphnode cells. Treatment of rats with a single injection of myelin liposomes after recovery from the first clinical episode significantly reduced the severity of the relapses.
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PMID:Myelin-liposome protection against experimental autoimmune encephalomyelitis is associated with reduced neuroantigen-specific T-cell-mediated responses. 842 33

The toxicological properties of ISIS 3082, a phosphorothioate oligonucleotide, and five structurally related analogs of ISIS 3082, were examined in Balb/c mice. Comparisons were made between the uniform phosphorothioate oligonucleotide (ISIS 3082), and a 2' propoxy modified phosphodiester (ISIS 9044), a 2' propoxy phosphorothioate (ISIS 9045), a chimeric oligonucleotide comprised of 2' propoxy diester wings and phosphorothioate deoxy center (ISIS 9046), a 5' C18 amine phosphorothioate (ISIS 9047), or a 5' cholesterol modified phosphorothioate (ISIS 8005) oligonucleotide. Oligonucleotides were administered at 50 mg/kg by i.v. bolus injection (tail vein) every other day for 14 days. In general, the spectrum of alterations observed for ISIS 3082 and all of the analogs were relatively similar. Balb/c mice treated with ISIS 3082 were observed to have increases in liver transaminases and a decrease in triglycerides consistent with results from previous studies performed in CD-1 mice. Spleen weights were also increased in ISIS 3082-treated mice, but no histopathological alterations were noted. ISIS 9046 resulted in a toxicity profile that was very similar to that described for ISIS 3082 with the exception of a slightly lower cholesterol level. Alterations induced by ISIS 9045, ISIS 9047 and ISIS 8005 were qualitatively similar to ISIS 3082, but in general more pronounced, with greater reductions in cholesterol and platelet counts, or increases in blood urea nitrogen relative to ISIS 3082. Red blood cell (RBC) counts and hematocrit were also reduced in mice treated with ISIS 9046, ISIS 9047 and ISIS 8005 relative to the ISIS 3082 treatment group. Kupffer cell hypertrophy and basophilic inclusions in Kupffer cells were observed in mice treated with ISIS 9045, ISIS 9047 and ISIS 8005, but not in ISIS 3082-treated mice. A unique renal lesions was noted in mice treated with ISIS 9044 only that was characterized as mild atrophy of proximal convoluted tubules associated with interstitial fibrosis. With the exception of the renal lesions observed in ISIS 9044 treated mice, the toxicity profiles of various oligonucleotide analogs examined in this study were similar to that observed for ISIS 3082.
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PMID:Toxicological properties of several novel oligonucleotide analogs in mice. 905 Nov 10

In the present study an acidic polysaccharide ginsan, with a molecular weight of 150,000, devoid of lectin properties, was purified from Panax ginseng C.A. Meyer (Araliaceae). Ginsan induced the proliferation of T cells and B cells. Spleen cells became cytotoxic to a wide range of tumor cells without major histocompatibility complex-restriction after 4 or 5 days culture in vitro with ginsan. For the generation of these ginsan-activated killer (AK) cells adherent macrophages and CD4+ cells were needed as accessory cells. The generation of ginsan-AK cells was blocked in the presence of anti-IL-2, anti-IFN gamma, anti-IL-1 or anti-TNF alpha antibodies, showing the importance of these cytokines in the process. The surface phenotypes of the 4 day-cultured ginsan-AK cells was Thy1+, AsGM1+, CD8+, which is distinct from rIL-2 induced lymphokine activated killer (LAK) cells that were CD8. The ginsan also activated macrophages to produce reactive nitrogen intermediates and become tumoricidal. It also exhibited significant in vivo antitumor activity against B16 melanoma cells lines, and in the benzo(a)pyrene-induced autochthonous lung tumor model, at much lower doses than the maximum tolerate doses. Indeed, no mice died, which injected with ginsan at 1g/kg body weight intraperitoneally. In conclusion, 'ginsan' could potentially be an ideal nontoxic antineoplastic immunostimulator by activating multiple effector arms of the immune system.
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PMID:Activation of multiple effector pathways of immune system by the antineoplastic immunostimulator acidic polysaccharide ginsan isolated from Panax ginseng. 906 72

Rat neutrophil granulocytes isolated after intraperitoneal casein injection of the donors exhibit high cytotoxic efficacy in vitro against microfilariae of Litomosoides carinii in the presence of ivermectin. Optimum effects of 80-90% killing of microfilariae were obtained with 100 ng ivermectin per milliliter and a microfilariae: cell ratio of 1:100. Spleen cells killed approximately 30% of the microfilariae under these conditions. Cytotoxic effects were independent of any adherence of the cell to the larvae. In contrast to the effects of spleen cells, cytotoxicity of neutrophils completely abrogated when cells and targets were separated by a membrane impermeable for the cells, suggesting a very short-living mediator in the latter case. Correspondingly, cytotoxic effects of neutrophils were completely inhibited by the addition of the arginine analogues NG-monomethyl-L-arginine and L-canavanine, indicating the involvement of reactive nitrogen intermediates. The nitric oxide scavenger hemoglobin also protected the microfilariae. Several compounds which are known to interfere with reactive oxygen intermediates were ineffective. An excess of ferrous ions in the medium in the presence of a reducing agent significantly reduced the cytotoxic efficacy of neutrophils.
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PMID:Ivermectin-induced killing of microfilariae in vitro by neutrophils mediated by NO. 920 41

Phex is the gene whose mutation is the cause of X-linked hypophosphatemia in humans and mice. The organs expressing Phex in normal animals, and their possible sensitivity to stimulation by low phosphate diets, are unknown. In this study, Phex expression was measured in 6-wk-old normal B6C3H male and female mice and in 135 g Sprague-Dawley rats fed a normal phosphate diet or a low phosphate diet with deionized water ad libitum for 7 d. The animals were then anesthetized, and a variety of organs were collected and frozen in liquid nitrogen. Phex mRNA expression was measured in each organ by reverse transcription-polymerase chain reaction (RT-PCR) with primers specific for both Phex and glyceraldehyde-3-phosphate dehydrogenase (G3PDH). Southern blots were prepared, hybridized with 32P-labeled internal oligonucleotides, and quantified with a phosphor imager. The Phex/G3PDH ratio was computed, and the data were compiled as the mean +/- SEM. In these growing animals, the highest Phexexpression levels were found in the gonads, brain, and lung. In contrast, Phex expression in calvaria and femur was markedly less. Two significant changes were found in animals that were fed a low phosphate diet. Spleen showed a significant decrease in Phex mRNA levels on low phosphate diet (60+/-10% of normal P diet, n = 12/group, p = 0.002). The pituitary gland showed a significant increase in Phex expression with low phosphate diet (851+/-127% of G3PDH) over normal P diet (569+/-78%, n = 24 - 25/group, p = 0.03). No significant change was found in femur, calvaria, or a variety of soft tissues. In summary, Phex mRNA was found in most tissues examined. Expression levels varied by two orders of magnitude from highest to lowest with more in gonads, brain, and lung and with less in bone. Increased Phex mRNA was found in the pituitary gland of animals that were fed a low phosphate diet.
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PMID:MRNA expression of Phex in mice and rats: the effect of low phosphate diet. 1105 Oct 50

Oxymetholone is a synthetic androgen, structurally related to testosterone. It is currently used to treat anemias, but has also been abused as a performance enhancing anabolic steroid by the sport community. Concern about its suspected immunomodulatory properties provided the incentive for a detailed investigation into its effects on the mammalian immune system. In this study, male B6C3F1 mice were treated for 14 d with oxymetholone (0, 50, 150, and 300 mg/kg) by gastric intubation, then evaluated for immunotoxicity using a panel of immunotoxicity assays. Except for an increasing trend in kidney and liver weights, and a dose-dependent increase in serum blood urea nitrogen levels, no other signs of systemic toxicity were observed. Bone marrow DNA synthesis was reduced, though this did not translate into alterations in myeloid or monocyte colony forming units. Spleen B and T cell numbers, antibody response to sheep red blood cells, proliferative response to both mitogen and immunoglobulin receptor immunogens, and NK cell activity were all unaltered in mice treated with oxymetholone. Peritoneal macrophage activity was also unaffected by oxymetholone treatment. A 38% decrease in the spleen cell mixed leukocyte response, and a 15% decrease in cytotoxic T cell activity, measured in the highest oxymetholone treatment group, indicate that cell-mediated immunity was impaired following exposure. This immunomodulation did not however, translate into a change in host resistance to Listeria monocytogenes.
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PMID:Oxymetholone modulates cell-mediated immunity in male B6C3F1 mice. 1107 98

Yersinia enterocolitica serotype O9 may cause a persistent intestinal infection with few or no symptoms in humans and in BALB/c mice. The present study demonstrated profound alterations in the immune status of BALB/c mice infected with Y. enterocolitica O9. Infected mice developed splenomegaly and phenotypic analysis of spleen cells revealed increases in CD3+ total T cells, CD4+ helper T cells, CD8+ cytotoxic T cells and CD11b+ phagocytic cells. Spleen cells from infected mice exhibited impaired responses to mitogens and suppressed the proliferation of normal splenocytes in response to mitogens. Suppression of responses to concanavalin A and heat-killed yersiniae was associated with increased production of gamma interferon and reactive nitrogen intermediates. Y. enterocolitica-infected mice resisted challenge with a lethal dose of the intracellular pathogen Listeria monocytogenes. These findings suggest that infection of mice with Y. enterocolitica O9 induces gamma-interferon-secreting cells that promote macrophage activation, mediating resistance to infection with L. monocytogenes, and macrophage production of reactive nitrogen intermediates, which results in in vitro inhibition of lymphocyte response to mitogens.
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PMID:Intestinal infection of BALB/c mice with Yersinia enterocolitica O9 causes major modifications in phenotype and functions of spleen cells. 1170 Mar 68


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