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)

A modification of yield reduction assay for interferon was developed. The standard micromethod of inhibition of cytopathogenic effect (CPE) of vesicular stomatitis virus (VSV) was first applied and the amount of virus antigen released to the supernatant was then measured by a competitive enzyme immunoassay technique. This assay was four times more sensitive than the CPE inhibition method and was able to detect 0.50-0.25 international units/ml of human interferon-alpha and was also applicable to interferon-gamma determinations. It is a suitable method when small volumes of samples containing low levels of interferon are tested.
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PMID:An interferon assay based on yield reduction of vesicular stomatitis virus antigen measured by enzyme immunoassay. 629 75

RD-114 line is a human sarcoma cell line chronically infected with RD-114 retrovirus. Treatment of these cells with increasing doses of human interferon-alpha or -gamma resulted in increasing inhibition of RD-114 virus production. Surprisingly, the replication of vesicular stomatitis virus and encephalomyocarditis virus, in these cells and in the parental RD cells which are not infected with the retrovirus, was insensitive to interferon treatment. Unlike reported differences in other properties of interferon-alpha and interferon-gamma, there were no differences in their antiretroviral properties such as dose response, kinetics of establishment of the antiretroviral state, and kinetics of its dissipation upon removal of interferon.
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PMID:Human interferon-alpha-and-gamma-mediated inhibition of retrovirus production in the absence of an inhibitory effect on vesicular stomatitis virus and encephalomyocarditis virus replication in RD-114 cells. 629 8

The secretory (tumor necrosis factor, TNF-alpha; nitrite) and cellular response (mitochondrial respiration, TNF-alpha-independent tumoricidal activity) of a pure, lymphocyte-free population of resting, unprimed rat bone marrow-derived mononuclear phagocytes (BMM phi) to direct interaction with viruses, protozoa, and fungi was assessed and compared with that triggered by bacterial agents and interferon-gamma (IFN-gamma). Viruses (herpes simplex, vaccinia, poliomyelitis, vesicular stomatitis, lymphocytic choriomeningitis, Sendai), protozoa (Trypanosoma brucei, Giardia lamblia), and fungi (Penicillium, Trichosporon, Fusarium, Rhizopus, Aspergillus, Geotrichum species) affected primarily the secretion of TNF-alpha and mitochondrial respiration of BMM phi; their effects on the secretion of nitrite and on tumoricidal activity were at best marginal. Collectively, the macrophage response to viruses, protozoa, and fungi was less varied and less marked than that to bacterial agents (intact organisms, peptidoglycan, lipoteichoic acid, lipopolysaccharide) and IFN-gamma.
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PMID:Macrophage response to viruses, protozoa, and fungi: secretory and cellular activities induced in resting unprimed bone marrow-derived mononuclear phagocytes. 799 64

Human interferon-gamma (hIFN gamma) exhibits a number of biological effects, including antiviral activity in homologous cells. The antiviral activity of recombinant (r) hIFN gamma, estimated by inhibition of vesicular stomatitis virus yield, was potentiated up to 120-fold in human fibroblast (BG-9) cells exposed to free L-T4 (0.5 x 10(-10) mol/L). Thyroid hormone alone did not induce the antiviral state in BG-9 cells. L-T3 also potentiated the antiviral action of rhIFN gamma, but D-T4 and D-T3 were ineffective. The antiviral effect of hIFN alpha in BG-9 cells was not influenced by thyroid hormone. Exposure of rhIFN gamma-treated BG-9 cells to L-T4 for only 3 h was sufficient to potentiate hIFN gamma-mediated antiviral activity. Similar potentiation by L-T4 of the antiviral effect of rhIFN gamma in HeLa cell cultures was also observed. Although the mechanism of potentiation of rhIFN gamma action by thyroid hormone is incompletely understood, the absence of antiviral activity of thyroid hormone alone indicates that the iodothyronine effect does not depend upon hormonal action on genes able to be stimulated by IFN gamma.
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PMID:Thyroid hormone potentiates the antiviral action of interferon-gamma in cultured human cells. 802 54

We have used the recently cloned cDNA for canine interferon-gamma (IFN-gamma) to engineer bacteria to produce large amounts of the recombinant cytokine. The resulting protein can be recognized by monoclonal and polyclonal antibodies largely species specific for canine IFN-gamma. The purified recombinant IFN-gamma (rIFN-gamma) also had biological activity in vitro in three assay systems: (i) vesicular stomatitis virus plaque inhibition, (ii) class II major histocompatibility complex antigen upregulation on canine kidney parenchymal cells, and (iii) amplification of in vitro tissue-associated lymphoproliferation, all known to be effected by native IFN-gamma (nIFN-gamma). The availability of large amounts of active canine rIFN-gamma will be an important tool in studies of the role of this cytokine in the widely used experimental canine organ transplant model and also will be of diagnostic and therapeutic veterinary interest.
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PMID:Production and characterization of recombinant canine interferon-gamma from Escherichia coli. 850 60

Manganese superoxide dismutase (MnSOD) is induced by interferon-gamma (IFN-gamma) in various cell lines. To determine whether MnSOD plays a role in the antiviral action of IFN-gamma, we employed an antisense strategy to inhibit the expression of MnSOD in the human melanoma cell line, A375. Three antisense-containing clones that exhibited reduced induction of MnSOD were investigated with respect to their response to the antiviral protective effects of IFN-gamma and IFN-alpha. We observed a striking decrease in the ability of IFN-gamma to protect antisense clones from vesicular stomatitis virus infection (VSV). The IFN-alpha induced antiviral state was also impaired, but to a lesser degree than was observed with IFN-gamma. We excluded the possibility that these effects were caused by a higher sensitivity of the antisense cells to VSV itself and found that the antisense clones actually were less sensitive to VSV. Therefore, we conclude that MnSOD is involved in the establishment of the IFN-gamma-induced antiviral state and to a lesser degree in the antiviral actions of IFN-gamma.
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PMID:Antisense manganese superoxide dismutase mRNA inhibits the antiviral action of interferon-gamma and interferon-alpha. 864 Apr 53

Infusion of interleukin-12 (IL-12) enhances recovery from lethal experimental vesicular stomatitis virus (VSV) infection of the central nervous system (CNS). Interleukin-12 treatment resulted in: 1) increased survival frequency; 2) faster recovery from weight loss; 3) substantially decreased VSV titers in brain homogenates and diminished immunohistochemical detection of VSV antigens in tissue sections; 4) earlier and increased CNS expression of types 1, 2, and 3 nitric oxide synthase (NOS) and both major histocompatibility complex (MHC) class I and class II antigens; 5) earlier and increased blood and CNS levels of tumor necrosis factor-alpha (TNF-alpha) and interferon-gamma (IFN-gamma). These results suggest that IL-12 enhances recovery from VSV infection of the CNS.
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PMID:Interleukin-12 promotes recovery from viral encephalitis. 909 30

The interplay between viral infection and lipopolysaccharide (LPS) was studied. Infection with a noncytopathogenic virus, lymphocytic choriomeningitis virus (LCMV), was found to sensitize mice to low doses of LPS. In vivo, this hypersensitivity correlated with hyperproduction of tumor necrosis factor-alpha (TNF-alpha), and in vitro, LPS-stimulated splenic adherent cells produced increased amounts of TNF-alpha. Hyperproduction of TNF-alpha was temporally correlated with virus-induced production of interferon-gamma (IFN-gamma); only marginally increased IFN-gamma and TNF-alpha production was observed in LCMV-infected, T cell-deficient mice and in mice infected with vesicular stomatitis virus, a virus that induces much less T cell activation than does LCMV. Finally, LCMV infection was much less efficient in priming IFN-gamma knockout mice for hyperproduction of TNF-alpha. These findings indicate that clinically silent viral infections may induce hypersensitivity to LPS through T cell activation and subsequent production of IFN-gamma; this sensitizes monocytes/macrophages for hyperproduction of TNF-alpha.
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PMID:Sensitization to lipopolysaccharide in mice with asymptomatic viral infection: role of T cell-dependent production of interferon-gamma. 920 61

A cDNA encoding chicken interferon-gamma (chIFN-gamma) was cloned from a CD4+ T-cell hybridoma by reverse transcription-polymerase chain reaction (RT-PCR) and expressed in Escherichia coli, COS- and CEC-32 fibroblast cell lines. In general, recombinant chicken IFN-gamma (rchIFN-gamma) expressed in the COS- and CEC-32 cell lines showed high bioactivity in vitro. The kinetics of IFN-gamma gene expression were examined in concanavalin A (Con A)-activated spleen lymphocytes by Northern blot and RT-PCR. IFN-gamma mRNA was detected as early as 30 min after Con A activation, reached peak expression at 2 h and then decreased starting at 4 h post Con A activation. A rabbit serum made to a synthetic peptide of IFN-gamma immunoprecipitated a 60 kDa E. coli maltose-binding fusion protein of recombinant IFN-gamma (MBP-IFN) and a 26-27 kDa secreted protein from COS cells and Con A-activated spleen cells. IFN-gamma inhibited vesicular stomatitis virus (VSV) mediated cytotoxicity of chicken embryonic fibroblast (CEF) cells and upregulated the expression of many macrophage cell surface antigens, including class I and class II major histocompatibility complex (MHC) proteins. These results show that chicken IFN-gamma possesses anti-viral activity and immunoregulates macrophage activities.
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PMID:Expression and functional characterization of recombinant chicken interferon-gamma. 943 75

Caprine interferon-gamma (IFN-gamma) cDNA was cloned from mitogen stimulated peripheral blood mononuclear cell (PBMC) RNA utilizing the reverse transcription-polymerase chain reaction (RT-PCR). The cDNA open reading frame (ORF) is 498bp, encoding a putative 166 amino acid (aa) protein (19327Da). The predicted aa sequence homology of caprine IFN-gamma and the corresponding ovine, bovine and cervine cytokine is 98.8%, 95.2% and 92.8%, respectively. IFN-gamma cDNA was subcloned and expressed in two different plasmids under the control of either the human cytomegalovirus (CMV) immediate early promoter or the caprine arthritis-encephalitis virus long terminal repeat (CAEV LTR). Recombinant caprine IFN-gamma (rCaIFN-gamma) secreted by transfected COS-7 cells shared at least two antigenic epitopes with recombinant bovine IFN-gamma (rBoIFN-gamma) and exhibited biological activity in the vesicular stomatitis virus (VSV) cytopathic effect reduction assay. In-vivo expression of IFN-gamma cDNA promoted by the CAEV LTR was confirmed by the intramuscular (IM) injection of Balb/C mice with plasmid followed by Western blot analysis of mouse serum against purified rCaIFN-gamma produced in E. coli.
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PMID:Cloning and expression of caprine interferon-gamma. 952 37


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