Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038362 (stomatitis)
 8,852 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We wished to assay recombinant equine interferon-beta 1 (rEqIFN-beta 1) but could not obtain satisfactory results with previously described methods. Therefore, we developed a yield-reduction assay, using primary horse peripheral blood mononuclear cells (PBMC) with vesicular stomatitis virus (VSV) for challenge, which proved consistently satisfactory and highly sensitive. It is suggested that this method of assay may be useful for IFNs from other animals where problems are encountered.
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PMID:A method for the assay of "difficult" interferons exemplified with recombinant equine interferon-beta 1. 131 33

Interferon is known to induce antiviral mechanisms and to exert immunoregulatory capacities on various cell types. The antiviral capacity of recombinant equine interferon-beta 1 (rEqIFN-beta 1) is most sensitively monitored by indirect quantitation of multiplication of vesicular stomatitis virus (VSV) in blood cells of horses. As few as 0.5 pg rEqIFN-beta 1/ml can be assessed by means of 90% reduction of VSV-replication in whole blood (w.b.) as well as in isolated mononuclear blood cells (MNC) in spite of individual variations. The immunoregulatory influence of 20-50 pg rEqIFN-beta 1/ml is sufficient to cause at least a 50% reduction of mitogen-induced lymphocyte proliferation in MNC, while higher concentrations are needed in w.b. Of the mitogens tested the best stimulation of proliferation on the equine lymphoid cells was obtained with staphylococcal enterotoxin B (SEB). Release of reactive oxygen species (ROS) from phagocytic cells in w.b. or from isolated polymorphonuclear cells (PMN) as monitored by chemiluminescence (CL) does not seem suitable for evaluation of rEqIFN-beta 1-induced immunoregulation as only very high rEqIFN-beta 1-concentrations (10(3)-10(4) pg/ml) result in a minute increase (up to 20%) of CL. Comparative studies on w.b. and isolated leukocyte fractions from identical specimens of individual horses suggest that monitoring of antiviral and distinct immunoregulatory capacities of rEqIFN-beta 1 can be performed on w.b. without loss of information and sensitivity as compared to isolated MNC.
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PMID:Monitoring of effects induced by recombinant equine interferon-beta 1 in whole blood and separated fractions of peripheral blood of horses. 132 23

Equine interferon-beta 1 (EqIFN-beta 1) was purified from extracts of recombinant Escherichia coli by sequential chromatography on hydroxylapatite, anion-, and cation-exchangers. The resulting protein was greater than 98% pure as determined by sodium dodecylsulfate gel electrophoresis, gel permeation HPLC, and reverse-phase HPLC. Amino-terminal amino acid sequencing revealed that essentially all molecules contained an additional amino-terminal methionine. The specific antiviral activity of EqIFN-beta 1 determined on equine dermal fibroblasts challenged with vesicular stomatitis virus (VSV) was approximately 5 X 10(8) U/mg. Less than 0.001% of this activity was observed in antiviral assays using human (A549), murine (L-M), ovine (SCP), or bovine (MDBK and BT) cells challenged with VSV or encephalomyocarditis virus. A series of monoclonal murine IgG antibodies were developed which neutralize the antiviral activity of EqIFN-beta 1. None of these antibodies nor rabbit antiserum to EqIFN-beta 1 were able to neutralize human IFN-beta; antiserum to human IFN-beta did not neutralize EqIFN-beta 1. Two of the monoclonal antibodies were used to establish a rapid one-step solid-phase enzyme immunoassay for EqIFN-beta 1.
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PMID:Recombinant equine interferon-beta 1: purification and preliminary characterization. 220 Aug 32

Tumour necrosis factor (TNF) induces antiviral activity in HEp-2 cells. Virus yield reduction assays with vesicular stomatitis virus as challenging virus demonstrated that the antiviral state was more pronounced in confluent cultures under low serum conditions. A significant enhancement of the antiviral state was obtained by combining TNF with low concentrations of either interferon (IFN)-beta 1 or IFN-gamma. The reduction in virus yield was significantly higher than that expected from summation of the independent antiviral activities of either substance alone, i.e. TNF and IFN acted synergistically as antiviral agents. Synergism of TNF with IFN-beta or IFN-gamma appeared to be mediated by different pathways, since different requirements for pretreatment and different effects on oligo-2',5'-adenylate synthetase (2-5AS) induction were observed. Induction of 2-5AS by TNF could be shown to be an indirect event that was sensitive to an antiserum against natural IFN-beta 1.
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PMID:Antiviral activity of tumour necrosis factor. Synergism with interferons and induction of oligo-2',5'-adenylate synthetase. 246 15

Hamster sarcoma virus (HSV) transformation of Nil-8 fibroblasts is associated with an increase in the average size of N-acetyllactosamine (complex) type N-linked glycans due to an increase in both the average number of branches/chain and in the fraction of N-linked glycans containing poly(GlcNAc(beta 1,3) Gal-(beta 1,4)) (polylactosaminylglycan) chains. Analysis of glycopeptides from the envelope glycoproteins of Sindbis virus and vesicular stomatitis virus (VSV) grown in Nil-8 and Nil/HSV cells indicated that the transformation-associated shift to larger N-linked oligosaccharides selectively affects some glycosylation sites far more than others. Glycosylation of the Sindbis virus glycoproteins and of Asn-179 of VSV G was similar in Nil-8 and Nil/HSV cells; oligosaccharide processing generally did not proceed beyond the biantennary complex stage. In contrast, Asn-336 of VSV G carried primarily biantennary complex glycans in Nil-8-grown virus (ratio, triantennary, and larger to biantennary complex glycans (tri+/bi) = 0.5) but more highly branched structures in Nil/HSV-grown virus (tri+/bi = 8.1). All of the triantennary or larger oligosaccharides from Asn-336 of Nil/HSV-grown VSV G bound to leukoagglutinating phytohemagglutinin-agarose, indicating the presence of a branch attached to the Man3GlcNAc2 core via a beta 1,6-linked GlcNAc residue and suggesting that increased UDP-GlcNAc:alpha-D-mannoside beta 1,6-N-acetylglucosaminyl transferase V (GlcNAc transferase V) activity accompanied transformation. At least 20% of these leukoagglutinating phytohemagglutinin-binding oligosaccharides were sensitive to an enzyme specific for polylactosaminylglycan chains, Escherichia freundii endo-beta-galactosidase.
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PMID:Differential effects of oncogenic transformation on N-linked oligosaccharide processing at individual glycosylation sites of viral glycoproteins. 282 91

Recombinant plasmids pMTIF-beta 1A and pMTIF-beta 1B were constructed by fusing the metallothionein I promoter-regulatory region to the human beta 1 interferon (HuIFN-beta 1) gene. These linearized fusion genes were then introduced into mouse germ lines by zygote microinjection. The chromosomal integration and the germ line transmission of the injected DNA sequences in the resulting transgenic mice were detected by DNA dot blot and Southern transfer hybridizations. The sera of at least two strains of metallothionein/HuIFN transgenic mice were found to protect human WISH cells against vesicular stomatitis virus infection, and this activity could be neutralized by preincubation with anti-HuIFN-beta 1 antibody. These transgenic mice demonstrated significantly enhanced resistance to pseudorabies virus compared with nontransgenic mice when inoculated with pseudorabies virus. The level of resistance seemed to correlate with the concentrations of HuIFN-beta 1 in serum. These transgenic mice may be used as models to study IFN-induced responses and may serve as prototypes to generate disease-resistant animals.
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PMID:Enhanced viral resistance in transgenic mice expressing the human beta 1 interferon. 284 84

The biochemical and kinetic properties of UDP-GlcNAc:alpha-D-mannoside (GlcNAc to Man alpha 1,3) beta 1,2-N-acetylglucosaminyltransferase I (GlcNAc-TI) have been investigated in the Chinese hamster ovary glycosylation mutant Lec1A. Previous studies showed that, whereas Lec1A cells synthesize complex carbohydrates at levels consistent with partial GlcNAc-TI action, no GlcNAc-TI activity was detected in Lec1A cell-free extracts (Stanley, P., and Chaney, W. (1985) Mol. Cell. Biol. 5, 1204-1211). It is now reported that, under altered reaction conditions, GlcNAc-TI activity can be measured in Lec1A cell extracts. The GlcNAc-TI enzyme in Lec1A.2C has a pH optimum of 7.5 (compared with 6.25 for the parental enzyme) and apparent Km values for Man5GlcNAc2Asn and UDP-GlcNAc that are, respectively, 21- and 44-fold higher than the apparent Km values of GlcNAc-TI from parental Chinese hamster ovary cells. Two independent Lec1A mutants possess GlcNAc-TI activities with similarly altered biochemical and kinetic properties. In fact, under optimal assay conditions for each cell line, the level of GlcNAc-TI in Lec1A extracts is equal to that of parental Chinese hamster ovary cell extracts. Interestingly, the two glycosylation sites of the G glycoprotein of vesicular stomatitis virus are processed quite differently in Lec1A cells. The glycopeptide nearest the carboxyl-terminal appears to be a preferred substrate for the Lec1A GlcNAc-TI activity. The combined data suggest that the Lec1A mutation affects the gene that codes for GlcNAc-TI, giving rise to a structurally altered glycosyltransferase with different biochemical properties.
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PMID:Lec1A Chinese hamster ovary cell mutants appear to arise from a structural alteration in N-acetylglucosaminyltransferase I. 294 43

The expression in human fibroblasts of the beta 2-interferon (IFN-beta 2) gene, which is now recognized to be identical to the gene encoding B-cell differentiation factor BSF-2, is enhanced by several cytokines that affect cell growth (tumor necrosis factor, interleukin 1, platelet-derived growth factor, and beta 1-interferon). We have examined the possibility that IFN-beta 2 gene expression is regulated through activation, by diacylglycerol, of the protein kinase C pathway. The synthetic diacylglycerols 1,2-dioctanoylglycerol (diC8) and 1-oleoyl-2-acetylglycerol strongly enhanced IFN-beta 2, but not IFN-beta 1, gene expression in human fibroblasts (FS-4 strain). An increase in IFN-beta 2 mRNA level was detected within 15 min after addition of diC8 (290 microM) to FS-4 cells and was maximal approximately 20 hr later. An increase in IFN-beta 2 gene transcription was detected within 5 min of addition of diC8, and the rate of transcription was near-maximal by 15-30 min. The enhancement of IFN-beta 2 gene expression by diC8, interleukin 1, or tumor necrosis factor was not prevented by H8, a preferential inhibitor of cAMP- and cGMP-dependent protein kinases, but was blocked by H7, an inhibitor of protein kinase C as well as of cyclic nucleotide-dependent protein kinases. diC8 was found to protect FS-4 cells from the cytopathic effect of vesicular stomatitis virus; this protection was blocked by polyclonal or monoclonal antibodies that neutralize IFN-beta, suggesting that the antiviral effect was due to the secretion of IFN-beta 2 by the diC8-treated fibroblasts. The calcium ionophore A23187 (1-10 microM) also elicited an increase in the level of IFN-beta 2 mRNA in FS-4 fibroblasts; appropriate combinations of A23187 and diC8 had at least an additive effect in enhancing IFN-beta 2 mRNA levels. These results show that protein kinase C-activating or [Ca2+]-elevating agents rapidly increase the expression of the IFN-beta 2 gene in human fibroblasts.
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PMID:Rapid enhancement of beta 2-interferon/B-cell differentiation factor BSF-2 gene expression in human fibroblasts by diacylglycerols and the calcium ionophore A23187. 310 77

Glycoproteins synthesized by the Chinese hamster ovary cell mutants LEC11 and LEC12 carry the Lex determinant (Gal beta 1,4(Fuc alpha 1,3)GlcNAc), while those synthesized by LEC11 cells also carry the sialyl-Lex determinant (NeuAc alpha 2,3Gal beta 1,4(Fuc alpha 1,3)GlcNAc), and both mutants have been shown to possess a distinct alpha(1,3)-fucosyltransferase of the appropriate specificity to synthesize these determinants (Campbell, C., and Stanley, P. (1983) Cell 35, 303-309; Campbell, C., and Stanley, P. (1984), J. Biol. Chem. 259, 11208-11214; Howard, D. R., Fukuda, M., Fukuda, M. N., and Stanley, P. (1987) J. Biol. Chem. 262, 16830-16837). The LEC11 cells therefore provide a source of carbohydrates terminating in sialylated, fucosylated lactosamine, a relatively rare structure not previously characterized by 1H NMR spectroscopy when in association with an N-linked carbohydrate. In this paper we use a monoclonal antibody specific for Lex to show that the G glycoprotein of vesicular stomatitis virus (VSV) grown in LEC11 and LEC12 cells possesses the Lex determinant and that G from LEC11/VSV also possesses sialylated Lex. Biantennary carbohydrates purified from LEC11/VSV and LEC12/VSV were therefore used to examine the effects on the 1H NMR spectrum of the presence of alpha(1,3)-fucose residues on sialylated and unsialylated lactosamine units. Comparisons of one-dimensional spectra obtained at 500 MHz from LEC11/VSV and LEC12/VSV glycopeptides before and after neuraminidase treatment with spectra of biantennary carbohydrates lacking alpha(1,3)-fucose allowed the assignment of several new resonances. Resolution of certain signals and determinations of coupling constants were achieved by two-dimensional correlation spectroscopy (COSY) at 400 MHz and allowed the assignment of several more resonances in the one-dimensional spectrum.
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PMID:The LEC11 Chinese hamster ovary mutant synthesizes N-linked carbohydrates containing sialylated, fucosylated lactosamine units. Analysis by one- and two-dimensional 1H NMR spectroscopy. 340 33

Recombinant equine interferon-beta 1 (reqIFN-beta 1) induces an antiviral state in blood mononuclear cells (BMC) of horses. Maximal protection against replication of vesicular stomatitis virus is achieved 6 hours after treatment with IFN in vitro and in vivo. Duration of the protective effect depends on the dose of IFN in vitro and in vivo. Availability of reqIFN-beta 1 in cultures of BMC for up to 48 hours does not prolong the antiviral state. The protective effect on BMC after treatment with IFN has similar duration in vivo and in vitro. Monitoring of the effect of IFN in vivo is, thus, simplified because the antiviral state may be recorded by testing cells twice (ie, before and 6 hours after application of interferon). All further tests may be performed in vitro. Multiple administration of reqIFN-beta 1 do not prolong duration of the protective phases after each administration. Duration of the antiviral state depends only on the dose of reqIFN-beta 1.
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PMID:Kinetics of inhibition of replication of vesicular stomatitis virus in blood mononuclear cells of horses after in vitro and in vivo treatment with recombinant equine interferon-beta 1. 797 48


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