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Results for “Interferon Type I”

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At least 19 recordsLinked to original sources
PubMedDate not supplied

[The inhibition by interferon type I of the initial phase of experimental salmonellosis].

Using the bacteriological methods the level of the genus Salmonella representative histadhesion to intestinal mucosa was evaluated. Balb/c mice and Salmonella typhimurium 415 strain were used for investigation. Native homologous I type interferon was injected to experimental animals 24 before the experiment in a dose of 1000 U/mice. "False" interferon was administered to the control group animals. It was established that the level of Salmonella histadhesion in mice of the experimental group was an order less than in control. Study of the parameters of the process of Salmonella interaction with intestinal mucosa showed that the challenge dose of Salmonella typhimurium 24 after interferon injection must be 7 times higher for the control mice than for experimental ones. Thus, the barrier function of intestinal mucosa after administration of the native I type interferon in vivo increased 7 times.

Animals↗
PubMed2000

A unique ISRE, in the TATA-less human Isg20 promoter, confers IRF-1-mediated responsiveness to both interferon type I and type II.

Interferons (IFNs) encode a family of secreted proteins involved in a number of regulatory functions such as control of cell proliferation, differentiation and regulation of the immune system. Their diverse biological actions are thought to be mediated by the products of specific but usually overlapping sets of cellular genes induced in the target cells. We have recently isolated a human cDNA encoding a new nuclear bodies-associated protein (PML-NBs), which we have termed Isg20. In this report, we describe the cloning and functional characterization of the Isg20 promoter region and the identification of sequence elements and trans-acting factors implicated in its regulation. In the absence of any recognizable TATA or CAAT elements, Isg20 promoter basal activity is dependent upon the positive transcription factors Sp-1 and USF-1. Interestingly, we demonstrate that a unique interferon stimulated response element (ISRE) mediates both IFN type I and type II Isg20 induction in the absence of functional gamma-activated sequence. These inductions are strictly dependent upon of the IFN regulatory factor 1 (IRF-1). In addition, we show that the ISRE is also implicated in the constitutive transcriptional activity of Isg20 gene.

Base Sequence↗
PubMed2003

Is flavivirus resistance interferon type I-independent?

Interferon type I comprises a group of major virus-inducible host antiviral factors that control infection with a great number of human and animal viruses. They are ubiquitously expressed cytokines that interfere with virus replication within different cell types by activating a number of host genes and several parallel antiviral pathways. Two major intracellular actors of IFN-I-induced antiviral states are ribonucleic acid-dependent protein kinase and 2'-5'-oligoadenylate synthetases/RNase L, both being induced by IFN-I and activated by viral double stranded ribonucleic acid. In addition, Mx proteins and ribonucleic acid-specific adenosine deaminase have also been implicated in IFN-I-induced antiviral responses to some RNA viruses. Viruses, in turn, have evolved different strategies to escape a control imposed by IFN-I and by IFN-I-induced antiviral factors. The fatal outcome of virus infection as well as the efficiency of IFN-I-based antiviral therapies in its prevention, are determined by complex interactions between viral virulence factors and cellular antiviral IFN-I inducible factors. In the light of these facts and current knowledge on IFN-I involvement in flavivirus infection, I discuss a possible role of IFN-I signalling in resistance to flavivirus infection in a model of congenic mouse strains that express different levels of susceptibility/resistance to common flaviviruses. Specifically, this review emphasizes importance of fully operative 2'-5'-oligoadenylate synthetases/RNase L pathway for the IFN-I-induced stimulation of flavivirus resistance conferred by Flv.

2',5'-Oligoadenylate Synthetase↗
PubMed1992

[Interferon type I in protective body reactions in an experimental Klebsiella infection].

The study on mice with experimental generalized Klebsiella infection, carried out with the use of microbiologic, immunologic and pathomorphologic methods, revealed that the intraperitoneal injection of type I interferon into the animals prevented their death and led to the rapid elimination of the infective agent from their body, enhanced the phagocytic and metabolic activity of polymorphonuclear lymphocytes of their peritoneal exudate, decreased the manifestation of microcirculatory and dystrophic changes in the parenchyma of their internal organs.

Animals↗
PubMed1986

[Effect of interferon type I on the in vivo persistence of Salmonella typhimurium].

The influence of type I interferon on the persistence of S. typhimurium in the body of mice has been studied. The injection of the preparation of interferon has been shown to be conductive to the survival of the animals and to reduce the time of Salmonella persistence in the body. The injection of interferon enhances the phagocytic activity of macrophages in the peritoneal exudate of mice.

Animals↗
PubMed2003

[Place of consensus type interferon alpha in the management of chronic type C hepatitis].

This paper presents the results of clinical investigations of efficacy of consensus type interferon (Alfacon-1) in monotherapy, as well as in combination with ribavirin. A special indication for this kind of interferon are "difficult" patients with high virial load non-responders for previous treatment, as well as with recurrence of infection.

Antiviral Agents↗
PubMed1998

Chicken interferon types I and II enhance synergistically the antiviral state and nitric oxide secretion.

This report shows that chicken type I and type II interferons (IFNs), like their mammalian counterparts, act synergistically such that a mixture of the two has much greater activity than that expected from the separate contribution of each type. The degree of antiviral synergy was measured by virus plaque reduction and cytopathic effect (CPE) inhibition in both primary and secondary chicken embryo cell cultures. Mixtures of the two Ch-IFNs produced antiviral effects 3-10 times greater than that expected from strict additivity of each IFN acting alone. At high concentrations of IFN mixtures there was a qualitative shift to an exponential IFN action does-response curve that revealed synergistic effects greater than 100-fold. Synergy resulted even with mixtures containing less than 1 U/ml of either type of Ch-IFN. The antiviral effects developed more rapidly with mixtures than when type I or II Ch-IFN was used alone. Mixtures of the two types of Ch-IFN synergistically potentiated nitric oxide secretion in cells of the HD11 chicken macrophage line. Molecular mechanisms are cited that may account for synergy between type I and type II IFNs, and speculation is offered on the epidemiologic and therapeutic implications of synergy in vivo.

Animals↗
PubMed2006

Interferon type I receptor-deficient mice have altered disease symptoms in response to influenza virus.

The role of type I interferons (IFNs) in mediation of acute viral symptoms (fever, somnolence, anorexia, etc.) is unknown. To determine the role of type I IFN in selected symptom development, body temperature and sleep responses to a marginally lethal dose of X-31 influenza virus were examined in mice with a targeted mutation of the IFN receptor type I (IFN-RI knockouts) and compared to wild-type 129 SvEv control mice. Mice were monitored for 48 h to determine baseline temperature and sleep profiles prior to infection, and then for 9 days following infection. Hypothermic responses to virus were perceptible beginning at 64 h post-infection (PI) and were more marked in KO mice until 108 h, when hypothermia became more exaggerated in wild-type controls. Temperatures of wild-type mice continued to decline through day 9 while temperatures in IFN-RI KO mice stabilized. Time spent in non-rapid eye movement sleep (NREMS) increased in KO mice when hypothermia was marked and then returned to baseline levels, while NREMS continued to increase in wild-type mice through day 9. Other sleep parameters [time spent in rapid eye movement sleep (REMS), relative NREMS EEG slow wave activity, NREMS EEG power density] were all reduced in wild-type mice compared to KOs from days 3 to 8 while REMS low frequency EEG power density increased in wild-type relative to KOs. In conclusion, our results indicate that the presence of functional type I IFN slightly ameliorates disease symptoms early in the X-31 infection while exacerbating disease symptoms later in the infection.

Analysis of Variance↗
PubMed2004

Interferon type I gene expression in chronic hepatitis C.

Hepatitis C virus (HCV) frequently causes chronic liver disease. The cause of viral persistence might be an inappropriate type I interferon (IFN) induction. To analyze the host's IFN response in chronic hepatitis C, we measured the transcription level of type I IFN genes as well as type I IFN-regulated genes in liver tissue and corresponding blood samples from patients with chronic hepatitis C, nonviral liver diseases, and a suspected but later excluded liver disease. Competitive and real-time RT-PCR assays were used to quantify the messenger RNA (mRNA) levels of all known IFN-alpha, IFN-beta, and IFN-lambda genes and those of some IFN-regulated genes. We failed to detect any hepatic type I IFN mRNA induction, although liver tissue of chronic hepatitis C patients contained high numbers of some type I IFN-inducible effector mRNA molecules. Analysis of peripheral blood samples, however, showed a clear type I IFN induction. Parallel experiments employing HCV replicon cell lines revealed that replication of HCV RNA is not sufficient to induce any type I IFN nor to induce directly type I IFN-regulated genes such as MxA. In conclusion, our data provide evidence for the absence of an induction of type I IFN genes by HCV in the human liver and argue for a further development of type I IFN-based therapies.

Adolescent↗
PubMed1998

Induction of spermidine/spermine N1-acetyltransferase by interferon type I in cells of hematopoietic origin.

A number of novel genes activated by type I interferons (IFNs) were identified by differential display. Of five induced genes examined, four were of unknown function. However, one gene sequence was identical to the human spermidine/spermine N1-acetyltransferase, the rate-limiting enzyme in polyamine catabolism. This enzyme was induced by type I IFNs in a series of hematopoietic cell lines, including Daudi, HL-60, HPBMa, and Wil-2. No induction above constitutive levels occurred in a cell line of epithelial (ME180) or liver (HepG2) origin following treatment with type I IFN. Spermidine/spermine N1-acetyltransferase was not induced by IFN-gamma in Daudi or ME180 cells. That induction occurred not only at the level of transcription but also at the enzyme level was confirmed by direct enzyme assays. As the levels of polyamines are related to cell viability, we propose that induction of this enzyme by IFN may be directly related to the anti-proliferative response to type I IFNs.

Acetyltransferases↗
PubMed1999

[IFN-tau, a new interferon type I with antiretroviral activity].

Type I interferon (IFN) such as IFN-alpha have demonstrated relative efficiency in HIV-infected patients with Kaposi's sarcoma. Nevertheless, their clinical uses have been restricted by several major side effects. IFN-tau is a non-cytotoxic type I IFN. In the present manuscript, we described its in vitro effects towards HIV replication and its mode of action. IFN-tau is a potent antiviral molecule that interferes with an early step of HIV biological cycle. Moreover, it induces IL-6 synthesis by macrophages, and this cytokine favorises its antiviral efficacy, probably by amplifying the induction of 2', 5'OAS and RNase L. Altogether, these results confirm the interest of IFN-tau as adjuvant therapy in HIV infection, and more particularly in HIV/HCV-infected patients.

Animals↗
PubMed1999

A bioassay for interferon type I based on inhibition of Sendai virus growth.

The expression of type I interferons (IFNs) in eukaryotic cells represents a first line of defense against viral infection. Cells pretreated by IFNs do not support viral replication and are protected from virus-induced cell destruction. A challenge of IFN-pretreated cells with vesicular stomatitis virus (VSV) is frequently used to quantitate this cytokine because, on the one hand, the replication of VSV is highly sensitive to IFNs and, on the other hand, in unprotected cells this virus induces a rapid cytopathic effect that can readily be quantified. However, as VSV may infect humans and is known to cause severe disease in a variety of animal species, this virus must be considered a biohazard. In this paper, we describe a bioassay for bovine IFN using Sendai virus, a paramyxovirus that grows readily in MDBK cells yet is released from these cells in a non-infectious form. The sensitivity and dynamic range of this assay are similar to those of the popular VSV-based IFN assay. We demonstrate that the Sendai-virus-based IFN assay permits rapid quantitation of recombinant bovine type I IFN, and also of native type I IFNs which are present in the supernatants of monocyte-derived macrophages infected with various pathogens. In view of the possible artifacts induced by viruses in samples to be assayed for IFN activity, we evaluated several methods of virus inactivation. Treatment with beta-propiolactone led to virus inactivation without affecting the bioactivity of IFNs as detected in the Sendai-virus-based assay.

Animals↗
PubMed1991

[The protective action of interferon type I in experimental Salmonella infection].

The effect of interferon, type 1, on the course of Salmonella infection in mice has been studied. The study has shown that the injection of homologous interferon of type 1 leads to the rapid elimination of the infective agent from the blood and organs of infected mice. Morphological study has shown that the injection of the preparations of interferon of type 1 may diminish pathological changes in the organs of the infected animals and the coagulation system of their blood.

Animals↗
PubMed2005

Sleep and body temperature responses in an acute viral infection model are altered in interferon type I receptor-deficient mice.

Type I interferons (IFNs) include IFNalpha and IFNbeta, both of which are elevated in acute viral infections and both of which have been shown to induce symptoms such as fever and somnolence when administered in pharmacological doses. To investigate the role of type I IFNs in mediation of acute respiratory viral symptoms we examined sleep and body temperature responses in mice with a targeted mutation of the IFN receptor type I (IFN-RI knockouts). IFN-RI knockouts (KOs) or wild-type 129 SvEv controls were challenged intratracheally (IT) with combined poly[rI.rC] (synthetic double-stranded RNA) and IFNgamma, a model that simulates an acute viral infection with respect to body temperature and locomotor activity responses. Control mice of both strains were treated with IT IFNgamma alone. Hypothermic responses to IT poly[rI.rC]/IFNgamma were more exaggerated in the IFN-RI KO mice than in wild-type. The non-rapid eye movement sleep (NREMS) response to IT poly[rI.rC]/IFNgamma was increased earlier in the IFN-RI KO mice than in wild-type, though the total time spent in NREMS was reduced in the KOs compared to wild-type and the return to baseline NREMS was faster in the KOs. The quality of NREMS also was altered more extensively in the wild-type than in the KO mice. Spontaneous rapid eye movement sleep (REMS) was suppressed in IFN-RI KOs as previously reported, but was not substantially altered in either mouse strain by IT poly[rI.rC]/IFNgamma challenge. Our results implicate type I IFNs as inhibitors of the hypothermic response and enhancers of the NREMS response to IT poly[rI.rC]/IFNgamma, a model of acute viral infection.

Analysis of Variance↗
PubMed2004

Interferon type I response in porcine reproductive and respiratory syndrome virus-infected MARC-145 cells.

Infection by porcine reproductive and respiratory syndrome virus (PRRSV) results in a weak induction of the innate immune response. There are many genes that collectively comprise this response and the extent to which each gene responds to PRRSV infection is unclear and warrants further investigation. To this end, we have utilized real-time PCR using SYBR Green I dye-based detection to quantify transcript abundance of the type I interferons (IFN-alpha and -beta) and IFN-beta transcriptional enhanceasome genes. In MARC-145 cells, both IFN-alpha and -beta transcript abundance were unaffected by PRRSV infection. However, stimulation of MARC-145 cells by exogenous double-stranded RNA, resulted in significant increases in transcript abundance of both IFN-alpha and -beta as well as IFN-beta enhanceasome components, indicating that a type I IFN response could be induced in these cells. The double-stranded RNA induction of type I IFN transcription was significantly inhibited by dual-exposure with PRRSV. These results suggest that PRRSV infection directly interferes with type I IFN transcriptional activation early in its pathway, at the level of IFN-beta gene transcription.

Animals↗
PubMed1999

Dimerization of the interferon type I receptor IFNaR2-2 is sufficient for induction of interferon effector genes but not for full antiviral activity.

We constructed chimeric receptors wherein the extracellular domain of the erythropoietin receptor (EpoR) was fused to the transmembrane and intracellular domains of the interferon (IFN) type I receptor subunits, IFNaR1 or IFNaR2-2. Transfection into 2fTGH and Tyk2-deficient 11,1 cells showed that EpoR/IFNaR2-2 alone was able to transduce a signal upon stimulation with erythropoietin (Epo), as judged by induction of the interferon type I-inducible 6-16 promoter. In contrast, protection against infection with encephalomyocarditis virus or vesicular stomatitis virus was reduced or absent, respectively. To further investigate the role of IFNaR1 in the induction of an antiviral state, we analyzed the Epo- versus IFNalpha-induced transcription of a set of genes, involved in antiviral protection. Up to 24 h after stimulation with Epo or IFNalpha, comparable transcription of the p56, dsRNA-dependent protein kinase, 2'-5'A synthetase, and MxA genes was seen. However, at later time points, only in the case of Epo induction, a sharp decrease of mRNA levels was observed. Western blotting analysis of dsRNA-dependent protein kinase showed a similar pattern at the protein level. Taken together, our results imply a role for IFNaR1 in the induction of sustained mRNA and protein levels that are likely required for optimal antiviral activity.

Alkaline Phosphatase↗