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)

Antiviral activities of a recombinant feline interferon (rFeIFN) KT-80 were evaluated against feline enteropathogenic viruses in feline and canine cell lines. Sensitivity to antiviral activities of the rFeIFN varied with cell types; Felis catus whole fetus (fcwf-4) cells were more sensitive than Crandell feline kidney cells, but no sensitivity was found for Madin-Darby canine kidney cells when vesicular stomatitis virus was used as a challenge virus. Reductions were generally IFN dose-dependent and were more consistent when the cells were continuously treated with the rFeIFN than when they were pretreated only before viral challenge. Compared with each virus control culture of fcwf-4 cells, yields of rotavirus, feline panleukopenia virus (FPLV), feline calicivirus and feline infectious peritonitis coronavirus were reduced by ranges of 1.3 to < or = 3.1 log10, 0.6 to 1.6 log2, 0.8 to 3.7 log10 and 0.5 to 0.6 log10, respectively, in the cultures continuously treated with 10 to 10000 U of the rFeIFN. The yield reduction of FPLV was considered to be in part attributable to inhibition of cell growth by the rFeIFN supplemented in the medium.
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PMID:Inhibitory effects of recombinant feline interferon on the replication of feline enteropathogenic viruses in vitro. 751 37

The hyper-IgD syndrome is a rare entity characterized by early onset of attacks of periodic fever. All patients have an elevated serum IgD (> 100 U/ml). Symptoms during attacks include joint involvements (arthralgias/arthritis), abdominal complaints (vomiting, pain, diarrhoea), skin lesions, swollen lymph nodes, and headache. In 1992 an International hyper-IgD study group was established, and to date the diagnosis has been made in 60, mainly European patients; 14 come from France. The disorder occurs in families and is transmitted by autosomal recessive inheritance. Linkage studies indicate that the gene encoding for familial Mediterranean fever is different from the gene for the hyper-IgD syndrome. In children the hyper-IgD syndrome should be distinguished from two other periodic febrile disorders. CINCA (chronic inflammatory, neurological, cutaneous and articular syndrome) and FAPA (periodic fever, adenopathies, pharyngitis, and aphtous stomatitis) share some symptoms with the hyper-IgD syndrome but in these syndromes serum IgD is normal. The pathogenesis remains to be elucidated but during attacks all patients have an acute-phase response with elevated C-reactive protein concentrations. During the febrile episodes, the inflammatory cytokines such as IL-6 TNF alpha, IFN gamma are increased together with natural occurring inhibitors such as IL-1ra and sTNFr. There is no therapy for the syndrome and patients will experience attacks during their entire life although frequency and severity tend to diminish with age.
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PMID:[Hyperimmunoglobulin D syndrome]. 756 50

Between May 1990 and April 1994, eleven patients with metastatic renal cell carcinoma received a combination therapy with interferon-alpha (IFN alpha) and 5-fluorouracil (5FU). IFN was administered intramuscularly six or ten million units three times per week for 4 weeks and 300 mg/m2 of 5FU was administered by continuous intravenous infusion daily for 4 weeks. Of 8 evaluable patients, two had a partial response (25%) two had a minor response (25%), and two had a stable disease (25%). The common side effects of the regimen were flu-like symptoms (91%), mucositis (64%) and leukopenia (75%). Three patients refused this therapy because of severe mucositis or stomatitis. Although the combination of IFN and 5FU in patients with metastatic renal cell carcinoma had some efficacy, this regimen had severe toxicity especially for the gastrointestinal (GI) tract. None of the patients could be administered the initially scheduled dosage of 500 mg/m2 of 5FU. The dose limiting factor of this regimen is considered to be GI symptoms.
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PMID:[Combination therapy with interferon-alpha and continuous infusion of 5-fluorouracil for advanced renal cell carcinoma]. 766 81

MxA is an IFN-induced human protein which is located in the cytoplasm of induced cells. MxA makes the cells resistant to infection by influenza and vesicular stomatitis viruses. In the present work we used baculovirus expression system to produce MxA protein. The protein was purified to homogeneity and highly specific polyclonal anti-MxA antibodies were prepared. In human mononuclear cells, and A549 lung carcinoma cells expression of MxA protein is induced by very low (< 1 IU/ml) doses of leukocyte IFN-alpha (nIFN-alpha), whereas IFN-gamma does not seem to induce it or potentiate the induction by IFN-alpha. In mononuclear cells stimulated with high doses of leukocyte IFN-alpha concentrations, the amount of MxA mRNA was induced 10-fold at 4 h after IFN induction and up to 10-fold higher MxA protein levels were observed at 24-48 h postinduction. The gene can be reinduced by IFN-alpha 24 h after the initial induction suggesting for a lack of negative feedback after this time point. The protein is very stable, the half-life being approximately 2.3 days. Flow cytometric analysis revealed that monocytes have higher basal and induced MxA protein levels than lymphocytes but the dose-dependency of MxA expression is very similar in both cell types. Granulocytes are producing very low amounts of MxA protein.
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PMID:Control of IFN-inducible MxA gene expression in human cells. 767 92

Interferon-gamma (IFN-gamma) and a type I IFN (spI IFN) are transiently coexpressed by trophoblastic cells of pig conceptuses at implantation between day 12 and day 20 of gestation. The local effects of these trophoblastic IFNs were examined on endometrial cells and on trophoblast by measuring antiviral activity and the induction of (2',5')-oligoadenylate synthetase activity. Trophoblastic vesicles were shown to be susceptible to infection by vesicular stomatitis virus and transmissible gastroenteritis virus. Vesicular stomatitis virus multiplied by about 1000 times in trophoblastic vesicles, and endogenous trophoblastic IFNs or exogenous recombinant IFN-gamma or spI IFN had no effect on virus production. No (2',5')-oligoadenylate synthetase activity could be measured on the trophoblast, even after treatment with IFN-gamma or spI IFN. These results clearly show that trophoblastic IFNs cannot induce antiviral resistance or (2',5')-oligoadenylate synthetase activity in the trophoblast, suggesting that these IFNs have no autocrine function. Endometrial epithelial and stromal cells in primary cultures displayed distinct sensitivity to the antiviral effect of IFN-gamma and spI IFN. Stromal fibroblasts were highly sensitive to spI IFN but weakly sensitive to IFN-gamma; epithelial cells were sensitive to both IFNs. The same sensitivity pattern was obtained when measuring the (2',5')-oligoadenylate synthetase activity. Flushing fluid, containing IFN-gamma and type I IFN, was a potent inducer of antiviral effect and (2',5')-oligoadenylate synthetase activity. It is therefore postulated that the endometrial epithelium is the most likely target of trophoblastic IFNs. It is possible that these IFNs play a role in the viral protection of conceptuses.
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PMID:Paracrine activities of porcine trophoblastic interferons. 779 12

The role of innate, alpha/beta interferon (IFN-alpha/beta)-dependent protection versus specific antibody-mediated protection against vesicular stomatitis virus (VSV) was evaluated in IFN-alpha/beta receptor-deficient mice (IFN-alpha/beta R0/0 mice). VSV is a close relative to rabies virus that causes neurological disease in mice. In contrast to normal mice, IFN-alpha/beta R0/0 mice were highly susceptible to infection with VSV because of ubiquitous high viral replication. Adoptive transfer experiments showed that neutralizing antibodies against the glycoprotein of VSV (VSV-G) protected these mice efficiently against systemic infection and against peripheral subcutaneous infection but protected only to a limited degree against intranasal infection with VSV. In contrast, VSV-specific T cells or antibodies specific for the nucleoprotein of VSV (VSV-N) were unable to protect IFN-alpha/beta R0/0 mice against VSV. These results demonstrate that mice are extremely sensitive to VSV if IFN-alpha/beta is not functional and that under these conditions, neutralizing antibody responses mediate efficient protection, but apparently only against extraneuronal infection.
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PMID:Antiviral protection by vesicular stomatitis virus-specific antibodies in alpha/beta interferon receptor-deficient mice. 788 63

We have previously shown that murine interferon gamma (IFN gamma) and its C-terminal peptide, muIFN gamma (95-133), bind to a region on the cytoplasmic domain of the IFN gamma receptor contained in the synthetic peptide, MIR(253-287). This region of the murine receptor bears considerable homology (approximately 80%) to its human counterpart. Here we report that not only do human IFN gamma and the human IFN gamma C-terminal peptide, huIFN gamma(95-134), bind to the cytoplasmic domain of the human IFN gamma receptor, but also that this interaction is species non-specific. MuIFN gamma(95-133) binds to human IFN gamma receptor cytoplasmic peptide HIR(252-291), and huIFN gamma(95-133) binds to MIR(253-287). Furthermore, treatment of murine macrophage cell lines with C-terminal peptides of either murine or human IFN gamma results in 10-fold upregulation of MHC class II molecule expression and increased resistance to infection with vesicular stomatitis virus (VSV) (10(6)-10(9)-fold reduction in yield). These data suggest a direct role for the C-terminus of IFN gamma in the initiation of intracellular signalling processes and may be indicative of a more general mechanism of action for extracellular signalling molecules.
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PMID:The C-terminus of IFN gamma is sufficient for intracellular function. 794 13

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

The previously cloned human interferon alpha/beta (Hu-IFN-alpha/beta; Type I interferon) receptor cDNA appears to be only one component of a receptor complex since expression of the cDNA in mouse cells confers sensitivity only to Hu-IFN-alpha B2, but a monoclonal antibody against this cloned receptor subunit inhibits biological activities of Hu-IFN-alpha A, Hu-IFN-alpha B2, Hu-IFN-omega, and Hu-IFN-beta. Here we report that a yeast artificial chromosome (YAC) containing a segment of human chromosome 21 introduced into Chinese hamster ovary (CHO) cells confers upon these cells a greatly enhanced response to Hu-IFN-alpha A and Hu-IFN-alpha B2 as well as an increased response to Hu-IFN-omega, Hu-IFN-alpha A/D(Bgl), andd Hu-IFN-beta. These responses were measured by induction of class I MHC antigens and by protection against encephalomyocarditis virus and vesicular stomatitis virus. Furthermore, these cells exhibit specific high affinity binding of Hu-IFN-alpha A and Hu-IFN-alpha B2, Hu-IFN-beta, and Hu-IFN-omega. The results indicate that all the genes necessary to reconstitute a biologically active Type I human IFN receptor complex are located within the human DNA insert of this YAC clone.
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PMID:Expression of a functional human type I interferon receptor in hamster cells: application of functional yeast artificial chromosome (YAC) screening. 802 72

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


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