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Query: UMLS:C0038187 (starvation)
 24,951 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Human lymphoid cell lines were studied as an experimental model for the spontaneous or induced occurrence of tuburloreticular structures (TRS). It was possible to induce TRS after culturing the EB-3 cell line with 20 mug/ml bromodeoxyuridine (BrUdR) during 96 h. Starvation, culturing at lower temperature (32 degrees) or inhibition of DNA synthesis did not give rise to the production of TRS. The response to BrUdR could be blocked with 60 mug/ml thymidine but not with 60 mug/ml deoxycytidine. The addition of 5 mug/ml cytarabine or the removal of BrUdR at different times resulted in inhibition of TRS induction, indicating that BrUdR had to be incorporated into DNA during at least 48 h. After incorporation, neither the presence of BrUdR nor DNA synthesis was necessary for the production of TRS. These experiments and the finding that in the cell line IHTC-33, which does not produce Epstein-Barr virus associated antigens, TRS were spontaneously present, exclude a correlation between TRS and these antigens. However, the induction of TRS by BrUdR may be related to the activation of another (latent) virus.
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PMID:Tubuloreticular structures in human lymphoid cell lines. A cell biological study. 17 83

The absence of erythrocytic adenosine deaminase (ADA) or purine nucleoside phosphorylase (PNP) has been associated with severe immunodeficiency disease in children. We have developed a cell culture model to study the possible relationships between purine salvage enzymes and immunologic function using an established T cell lymphosarcoma (S49) and a potent inhibitor of ADA, erythro-9(2-hydroxy-3-nonyl) adenine (EHNA). Wild-type S49 cells are killed by dexamethasone or dbc AMP, and adenosine (5 muM) in the presence of an ADA inhibitor (6 muM EHNA) also prevents the growth of and kills these S49 cells. It has been proposed that adenosine is toxic to lymphoid cells by virtue of its ability to increase the intracellular concentrations of cyclic AMP. We examined the sensitivity of three mutants of S49 cells, with distinctive defects in some component of cyclic AMP metabolism or action, to killing by adenosine and EHNA. All three mutants are resistant to killing by isoproterenol or cholera toxin and two are resistant to dbc AMP itself, but all are sensitive to killing by adenosine and EHNA. Similarly, two dexamethasone-resistant S49 mutants are as sensitive to adenosine and EHNA as are the wildtype cells. We have also simulated the purine nucleoside phosphorylase deficiency in S49 cells by adding inosine and adenosine to the growth medium. In the presence of EHNA or inosine, the toxic effects of adenosine can be partially reversed by addition of (10-20 muM) uridine, an observation suggesting that adenosine is toxic as the result of its inducing pyrimidine starvation.
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PMID:Characterization of a cell culture model for the study of adenosine deaminase- and purine nucleoside phosphorylase-deficient immunologic disease. 18 61

The effect of 24 and 48 hours of food and water deprivation on ascorbic acid, liver, leukocyte counts and internal lymphoid organ weights of crossbred chicks was examined. Starvation caused an increase in plasma ascorbic acid level, a significant decrease in leucocyte count in peripheral blood, significant loss in body weight and a profound loss in liver, bursa of fabricius, spleen and thymus weights. Deprived chicks were I.V. injected with Escherichia coli dead bacteria and sheep red blood cells at different times before and after onset of deprivation. Blood samples were taken 3, 6, and 12 days thereafter. A lower antibody titer was found on the 6th day post vaccination in the groups where deprivation started on the day before or on the day of vaccination.
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PMID:The effect of starvation on antibody production of chicks. 34 87

The effects of starvation on the cellular immune response of C58/Wm mice to syngeneic malignant lymphoid cells (1b cells) were studied. Mice were starved 1-3 days before or after immunization. The capacity of starved animals to survive immunization was used to quantify immunosuppression. When starvation bracketed immunization by -1 to +1 days, only 2 of 23 mice survived primary immunization, compared with 100% survival for nonstarved controls. A 2-day period of starvation +1 to +7 days after primary immunization reduced survival about 30%. For a test of the effect of starvation on the secondary immune response, mice were immunized, starved 2 days, and then challenged with viable lb cells. When mice were starved from -3 to +1 days before or after challenge, there was a 25-45% decrease in survival. Starvation caused a disproportionate depletion of lymphoid tissue elements. The proportional loss in the weight of the spleen and thymus was essentially twice as great as the loss in total body weight. The peripheral blood leukocyte count was reduced by about 20% when mice were starved 1 day and by approximately 50% when they were starved 2 days. When mice were starved 1-2 days, the differential leukocyte count did not shift and there was no significant change in the number of blood erythrocytes or in the hematocrit. Starvation for 2 days caused a 65-70% reduction in the number of viable mononuclear spleen cells. Starvation for 3 days caused about 90% reduction. Adoptive cell transfer experiments showed that the immunocompetence of individual spleen immunocytes was not reduced by starvation.
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PMID:Immune mechanisms in leukemia: suppression of cellular immunity by starvation. 118 12

The knowledge about the differentiation of basophilic leukocytes is fragmentary. This report discusses a detailed phenotypic characterization of molecular markers for hematopoietic differentiation in a basophilic leukemia cell line, KU812. The expression of markers for lymphoid, erythroid, neutrophil, eosinophil, monocytic, megakaryocytic, mast cell and basophil differentiation was analyzed at the mRNA level by Northern blots in the KU812 cells, and for reference, in a panel of human cell lines representative of the different hematopoietic differentiation lineages. KU812 was found to express a number of mast cell and basophil-related proteins, i.e. mast cell tryptase, mast cell carboxypeptidase A, high-affinity immunoglobulin (IgE) receptor alpha and gamma chains and the core protein for heparin and chondroitin sulphate synthesis. We found no expression of a number of monocyte/-macrophage or neutrophil leukocyte markers except for lysozyme. From earlier studies, it has been shown that lysozyme is not expressed in murine mucosal mast cell lines. This finding, together with the expression of the mast cell carboxypeptidase in KU812 might distinguish the phenotype of this cell line from that typical of mucosal mast cell lines in rodents. We found a low level of expression of the eosinophil and basophil marker, major basic protein, which might indicate a relationship between basophils and eosinophils. No expression is, however, detected with the eosinophil-specific markers eosinophil cationic protein, eosinophil-derived neurotoxin or eosinophil peroxidase. We also report an extensive screening for inducers of basophilic differentiation of the KU812 cells. The most efficient protocol of induction included serum starvation which led to a dramatic increase in a number of markers specific for mast cells and basophils such as tryptase, carboxypeptidase A and the heparin core protein. Finally, diisopropylfluorophosphate analysis of total protein extracts from KU812 show four labeled protein bands with sodium dodecyl sulfate-polyacrylamide gel electrophoresis, indicating that this cell line expresses at least three previously undescribed serine proteases of which one or more could be a potential basophil-specific marker(s).
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PMID:Phenotypic characterization of KU812, a cell line identified as an immature human basophilic leukocyte. 163 3

The expression of c-myb mRNA is differentially regulated in murine B lymphoid tumors such that B cell lymphomas and plasmacytomas contain significantly less c-myb mRNA than pre-B cell lymphomas. To examine the low level of c-myb mRNA expression in the murine B cell lymphoma cell line BCL1, nonessential amino acid starvation was used to block these cells in a G1 state. When BCL1 cells were released from this block, a 7- to 10-fold increase in c-myb mRNA was detected in late G1 and S phase cells relative to that detected in exponentially growing BCL1 cells. This increase was not inhibited by aphidicolin. To determine whether cell cycle regulation of c-myb mRNA expression occurred during exponential growth in both murine pre-B cell lymphoma and B cell lymphoma cell lines, elutriation was used to separate exponentially growing cell populations. An increase in c-myb mRNA expression was seen in late G1 and S phase fractions from B cell lymphoma cell lines. In contrast, c-myb mRNA levels remained constant in elutriation fractions isolated from pre-B cell lymphoma cell lines. Expression of c-myb mRNA was not detected in exponentially growing or in Go serum-stimulated murine fibroblasts. These results indicate that constitutive vs cell cycle regulation of c-myb mRNA expression is related to the state of differentiation in murine B lymphoid tumors and suggest that a switch in regulation may occur during normal B cell development.
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PMID:Constitutive versus cell cycle regulation of c-myb mRNA expression correlates with developmental stages in murine B lymphoid tumors. 173 Aug 80

The effects of refeeding subsequent to starvation on the plasma cell population in the lamina propria of the small intestinal villi were studied in adult rats utilizing the immunohistochemical method to detect IgA, IgM and IgG. Under normal conditions of stimulation, intestinal plasma cells (IPC) occur only as a sparse population. However, the present study demonstrated that extensive hyperplasia of IPC could be induced by refeeding after starvation. Starvation for a period of 4 to 6 days alone produced only a small change in the IPC population. In contrast, refeeding subsequent to starvation (for 4 to 6 days) was accompanied by a large increase in the population of IPC: the proportions of these cells among the lamina propria cells often rose to more than 50% within 3 or 6 days. The large majority of the proliferating IPC were found to express IgA, whereas cells bearing IgM or IgG occurred in extremely small numbers in the lamina propria. The mechanism whereby extensive IPC hyperplasia can occur in response to refeeding after starvation is discussed in relation to the possible promotion of transmission of antigenic macromolecules across the mucosal barrier induced by this procedure. It is also suggested that the origin of the proliferating IPC may be correlated with the B cell precursors in the germinal centers of the Peyer's, patches, which are more resistant to starvation than other lymphoid cells.
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PMID:Effects of refeeding subsequent to starvation on the plasma cell population in the villous lamina propria of the rat small intestine. 206 77

The mechanism and cellular targets of mononuclear cell depletion were investigated in strains of mice susceptible or resistant to lethal infection with a virulent street rabies virus (SRV). Significant depletion was evident in the thymus of all infected animals at approximately 5 days postinfection and subsequently involved the spleen and lymph nodes in mice developing clinical signs of rabies. Immunofluorescent analyses of lymphocyte subsets in depleted spleens revealed that cell losses were non-selective since the relative proportions of K+, Thy-1+, Lyt-1+, and Lyt-2+ cells remained unchanged. Diminished expression of I-A membrane glycoproteins on spleen lymphocytes was noted, however, perhaps reflecting reduced availability of I-A-inducing lymphokines. Adrenal hormone toxicity was identified as the cause of mononuclear cell depletion in that mice adrenalectomized before SRV infection showed no evidence of lymphoid depletion. The failure of adrenalectomy to alter anti-rabies antibody responses or SRV lethality also indicates that involution of the lymphoid system is a consequence and not a cause of genetically controlled host susceptibility to SRV. The mechanism of adrenal gland stimulation in rabies-infected mice appears to involve a virus-induced dysfunction in the pituitary gland rather than a stress response to paralysis-induced starvation, based on results of kinetic studies on weight loss, appetite depression, and paralysis in these animals and previous reports of pituitary infection during rabies disease. The relationship of these observations to current theories on rabies virus pathogenicity is discussed.
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PMID:Murine susceptibility to street rabies virus is unrelated to induction of host lymphoid depletion. 232 81

An H-2-associated immune response gene which maps to the I-A subregion of the H-2 complex governs the ability of H-2 congenic mice to mount an antibody response to five phosphoproteins with molecular weights of 33,000, 29,000, 23,000, 17,000, and 16,000 when inoculated with BW5147, a spontaneous AKR T-cell leukemic cell line. The phosphoproteins are present in all tumor cell lines tested, including those of murine and human origins. The phosphoproteins are associated with the proliferative state of the cell as studied in many systems including growth stimulation of normal lymphoid cells with mitogens, interleukin 2 dependency for growth of a cloned T-cell line, cessation of proliferation by serum starvation of Swiss 3T3 fibroblasts, retention of the proliferative capacity of SV40-transformed 3T3 fibroblasts, and the differentiation and inhibition of proliferation of human promyelocytic leukemic cells. Phosphoproteins with molecular weights of 33,000, 29,000, 23,000, 17,000, and 16,000 are therefore not specific to a particular inducible cellular pathway but are associated with cell proliferation in general.
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PMID:Phosphoproteins recognized by an H-2-linked immune response gene and their association with cell proliferation. 309 5

The 78,000-dalton glucose-regulated protein (GRP78) and the immunoglobulin heavy-chain-binding protein (BiP) were shown to be the same protein by NH2-terminal sequence comparison. Immunoprecipitation of GRP78-BiP induced by glucose starvation and a temperature-sensitive mutation in a hamster fibroblast cell line demonstrated the association of GRP78-BiP with other cellular proteins. In both fibroblasts and lymphoid cells, GRP78-BiP was found to label with 32Pi and [3H]adenosine. Phosphoamino acid analysis demonstrated that GRP78-BiP is phosphorylated on serine and threonine residues. Conditions which induce increased production of GRP78-BiP resulted in decreased incorporation of 32Pi and [3H]adenosine into GRP78-BiP. Furthermore, we report here that the phosphorylated form of BiP resides in the endoplasmic reticulum and that BiP which is associated with heavy chains is not phosphorylated or labeled with [3H]adenosine, whereas free BiP is. This suggests that posttranslational modifications may be important in regulating the synthesis and binding of BiP.
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PMID:Identity of the immunoglobulin heavy-chain-binding protein with the 78,000-dalton glucose-regulated protein and the role of posttranslational modifications in its binding function. 314 86


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