Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:2.7.7.49 (reverse transcriptase)
31,746 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

While the role of cytokines in mediating injury during hind limb skeletal muscle ischemia followed by reperfusion has recently been described, the role of cytokines in myocardial infarction and ischemia/reperfusion have remained relatively unexplored. We hypothesize that cytokines play an important role in the regulation of postischemic myocardial inflammation. This study reports the temporal sequence of proinflammatory cytokine gene expression in postischemic/reperfused myocardium and localizes interleukin-1 beta (IL-1 beta) and tumor necrosis factor-alpha (TNF-alpha)-protein by immunostaining. Rats were subjected to either permanent left anterior descending (LAD) occlusion or to 35 minutes of LAD occlusion followed by reperfusion and sacrificed up to 7 days later. Rat-specific oligonucleotide probes were used to semiquantitatively assess the relative expression of mRNA for TNF-alpha, IL-1 beta, IL-2, IL-6, interferon-gamma (IFN-gamma), and transforming growth factor-beta 1 (TGF-beta 1) utilizing the reverse transcriptase-polymerase chain reaction amplification technique. Increased cardiac mRNA levels for all cytokines except IL-6 and IFN-gamma were measurable within 15 to 30 minutes of LAD occlusion and increased levels were generally sustained for 3 hours. During early reperfusion, mRNA levels for IL-6 and TGF-beta 1 were significantly reduced compared with permanent LAD occlusion. In both groups, cytokine mRNA levels all returned to baseline levels at 24 hours, while IL-1 beta, TNF-alpha, and TGF-beta 1 mRNA levels again rose significantly at 7 days only in animals with permanent LAD occlusion. Immunostaining for IL-1 beta and TNF-alpha protein revealed two patterns of reactivity: 1) microvascular staining for both IL-1 beta and TNF-alpha protein only in postischemic reperfused myocardium in early post-reperfusion time points; and 2) staining of infiltrating macrophages in healing infarct zones which was most prominent at 7 days after permanent LAD occlusion. These results provide evidence for local expression of cytokine mRNA in postischemic myocardium and suggest that regulation of local cytokine release is altered during the postischemic period.
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PMID:Cytokine mRNA expression in postischemic/reperfused myocardium. 785 52

Immunity to Brucella abortus crucially depends on antigen (Ag)-specific T-cell mediated activation of macrophages, which are the major effectors of cell-mediated killing of this organism. Ribosomal preparations have been used as vaccines against several pathogens, including B. abortus, conferring a high degree of protection. In the present study, we have examined the pattern of T-helper (Th) cell response from infected BALB/c mice after in vitro stimulation with recombinant (r) L7/L12 ribosomal protein or gamma-irradiated B. abortus. In addition to Ag-specific proliferation, CD4+ T cells were tested for interleukin-2 (IL-2), IL-4 and interferon-gamma (IFN-gamma) mRNA expression and secretion. Detection of cytokine transcripts and secreted cytokines was performed using reverse transcriptase (RT)-polymerase chain reaction (PCR) and specific ELISA assays. Primed CD4+ T cells proliferated to the recombinant protein or whole B. abortus. The functional cytokine profile of the proliferating cells was typical of a Th1 cell phenotype, as we detected transcripts for IL-2 and IFN-gamma but not IL-4. Among the cytokines analysed, only IFN-gamma produced in the Th cell culture supernatants was detected by ELISA when bacteria or recombinant protein were used. Thus, rL7/L12 ribosomal protein and gamma-irradiated B. abortus preferentially stimulated IFN-gamma-producing Th1 cells after in vitro stimulation. The results of this study provide for the first time an explanation of why ribosomal vaccines may protect against intracellular infections, and an experimental basis for identifying polypeptides from a pathogen which stimulates the desired cytokine profile and Th cell response crucial for the design of genetically engineered candidate vaccines.
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PMID:Recombinant L7/L12 ribosomal protein and gamma-irradiated Brucella abortus induce a T-helper 1 subset response from murine CD4+ T cells. 787 46

Kupffer cells are known to produce tumor necrosis factor-alpha upon stimulation with endotoxin or viruses. This tumor necrosis factor-alpha synthesis is suppressed by prostaglandin E2 or dexamethasone. Using Northern blotting and reverse transcriptase-polymerase chain reaction, it is demonstrated that endotoxin-induced tumor necrosis factor-alpha synthesis is blocked by prostaglandin E2 or dibutyryl 3':5'-cyclic adenosine monophosphate on the transcriptional level. Tumor necrosis factor-alpha itself suppressed endotoxin-evoked tumor necrosis factor-alpha mRNA expression when given in a narrow time interval with lipopolysaccharide. Interleukin-10 of human or mouse origin also inhibited the synthesis of tumor necrosis factor-alpha mRNA and protein when given more than 2 h prior to the endotoxin challenge. The suppressive effect of prostaglandin E2 lasted for more than 36 h while IL-10 blocked tumor necrosis factor-alpha production for barely 24 h. Dexamethasone reduced the endotoxin-induced tumor necrosis factor-alpha mRNA formation by approximately 50% only, although it led to nearly complete inhibition of the synthesis of the mature protein. Taken together with reverse transcriptase-polymerase chain reaction data revealing significant amounts of tumor necrosis factor-alpha mRNA in resting Kupffer cells, an additional posttranscriptional regulation of tumor necrosis factor-alpha synthesis has to be assumed. Tumor necrosis factor-alpha mRNA was not induced by interferon-gamma, interleukin-1 beta or interleukin-6 (the latter two cytokines are also synthesized by Kupffer cells), but a 24-h prestimulation of liver macrophages with interferon-gamma or phorbol ester had a modest priming effect.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Regulation of the mRNA expression for tumor necrosis factor-alpha in rat liver macrophages. 793 Apr 83

Normal human epidermis is a rich source of biologically active interleukin-1 alpha (IL-1 alpha). Keratinocytes both synthesize this cytokine and respond to it via cell surface receptors (IL-1R), suggesting that the IL-1 system may play an important role in normal epidermal physiology and inflammation. In this study, we have examined the expression of IL-1R in normal and psoriatic epidermis, as judged at a functional level by the capacity to bind 125I-labeled IL-1 alpha (the principal IL-1 species present in epidermis) and by immunostaining with antibodies specific for each species of IL-1R. IL-1R was not readily detectable by either technique in normal, freshly isolated human epidermis. However, in lesional psoriasis or normal epidermis after 24 hours of organ culture, expression of IL-1R was dramatically induced, especially in basal keratinocytes. Immunostaining and antibody blocking studies demonstrated the induced IL-1R to be the type II species, a nonsignal transducing molecule previously demonstrated only on leukocytes. The Ka of this receptor was comparable to that previously demonstrated in vitro. mRNA for both species of IL-1R could be demonstrated by reverse transcriptase-polymerase chain reaction in fresh and cultured epidermis. These in vivo findings were confirmed in culture, where normal human keratinocytes expressed few IL-1R at rest but large numbers of type II IL-1R after activation by phorbol ester or interferon-gamma. We conclude that under resting conditions, epidermal expression of IL-1R is low. However, the potential for keratinocytes in vivo to express large numbers of the nonsignal transducing type II IL-1R is evident from both organ cultured and psoriatic epidermis. The in vitro induction of keratinocyte IL-1R by interferon-gamma suggests that this cytokine may be involved in the induction of type II IL-1R in inflammatory skin disease. The presence of bioactive IL-1 in epidermis, coupled with the inducible expression of the decoy type II IL-1R, indicates the existence of a highly regulated system of autocrine stimulation of keratinocytes by IL-1.
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PMID:Detection of interleukin-1 receptors in human epidermis. Induction of the type II receptor after organ culture and in psoriasis. 797 38

In this study, we examined the impact of the predominantly Th2-type lymphokines interleukin 13 (IL-13) and interleukin 4 (IL-4) on acute infection of human bronchoalveolar macrophages with a macrophage-tropic isolate of human immunodeficiency virus type 1 (HIV-1). Addition of 0.01-10 ng of IL-4 or IL-13 per milliliters significantly blocked HIV-1 replication in infected cells, judging from levels of reverse transcriptase and p24 antigen in the supernatants of infected cells. Both IL-4 and IL-13 were almost as efficient as interferon-gamma (IFN-gamma) in preventing HIV-1 replication, when given in equivalent amounts. Moreover, neither IL-13 nor IL-4 interfered with the IFN-gamma-mediated enhancement of anti-HIV-1 activity in alveolar macrophages. Both IL-4 and IL-13 interfered with enhanced replication of HIV-1 in macrophages pulsed with the growth factor granulocyte-macrophage colony-stimulating factor (GM-CSF). Interleukin 13 also prevented HIV-1 release from peripheral blood mononuclear cells in a cocultivation experiment with feeder cells from a seronegative subject. These data suggest that Th2-derived lymphokines have significant anti-HIV-1 activity in cells of the macrophage lineage, although they may enhance the susceptibility of HIV-1-infected subjects to some opportunistic pathogens.
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PMID:Interleukin 13 and interleukin 4 protect bronchoalveolar macrophages from productive infection with human immunodeficiency virus type 1. 798 85

Treatment of monocytes with interferon-gamma 1 day before, or at the time of infection with human immunodeficiency virus type-1 (HIV-1) induced complete resistance in monocytes against HIV-1 infection. There was no evidence of viral RNA, proviral DNA, p24 antigen, or reverse transcriptase activity through 2 weeks after inoculation. Ultrastructural examination of these cells showed no detectable virus particles. When interferon-gamma was added to monocytes 1 to 3 days post-infection, virus integration occurred, but the viral expression was either ablated (1 day post-infection) or significantly inhibited (3 days post-infection). Treatment of monocytes with interferon-gamma before or after infection with HIV-1 produced significantly higher levels of tumor necrosis factor-alpha and interleukin-8 than untreated or uninfected monocytes. These results suggest that altered regulation of cytokines may mediate antiviral activity of interferon-gamma in monocytes.
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PMID:Interferon-gamma induces resistance in primary monocytes against human immunodeficiency virus type-1 infection. 800 12

Monocytes treated with 500 IU/ml human recombinant interferon-gamma (rIFN-gamma) 1 day before and continuously after human immunodeficiency virus (HIV) infection showed no evidence of virus replication 7 days after addition of the viral inoculum. There was no HIV-associated cytopathic effect, no reverse transcriptase (RT) activity or p24 detected in culture fluids, and no HIV RNA or DNA in cell lysates. Furthermore, no evidence of HIV infection was evident in replicate cultures in which all IFN-gamma was removed at 7 days and the cells were cultured for an additional 3 weeks without IFN-gamma. The 50% inhibitory dose for reduction of maximum RT activity in HIV-infected monocyte cultures was about 1 IU/ml IFN-gamma. No increase in HIV replication was evident in monocytes treated with IFN-gamma at any concentration (0 to 5000 IU/ml) or at any time (7 days before to 10 days after HIV infection). In side-by-side experiments with identical monocytes and HIV-1 stock, rIFN-gamma was 10 to 20 times more effective than rIFN-alpha 2b for induction of antiviral activity. With both interferons, significant antiviral activity was evident with monocytes treated 1 day before, at the time of, or up to 3 days after infection. At 7 to 10 days after infection (a time at which less than 20% of total cells were infected with HIV) addition of even high concentrations of IFN-alpha or IFN-gamma had no effect on virus replication. These data suggest that the principal action of IFN-alpha and IFN-gamma was directed against the fluid-phase virus. Cell-cell spread of infection within the HIV-infected monocyte culture and extent of virus replication in HIV-infected cells were not affected by interferon treatment.
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PMID:Interferon-gamma protects primary monocytes against infection with human immunodeficiency virus type 1. 808 9

Carboxylic esterases are widely distributed in hematopoietic cells. Monocytes express the esterase isoenzyme (termed 'monocyte-specific esterase', MSE) that can be inhibited by NaF in the alpha-naphthyl acetate cytochemical staining. We examined the expression of MSE in normal cells and primary and cultured leukemia-lymphoma cells. The MSE protein was demonstrated by isoelectric focusing (IEF); MSE mRNA expression was investigated by Northern blotting and reverse transcriptase-polymerase chain reaction (RT-PCR). The following samples were positive for MSE protein and Northern mRNA expression: 20/24 monocytic, 4/32 myeloid, and 1/20 erythroid-megakaryocytic leukemia cell lines, but none of the 112 lymphoid leukemia or lymphoma cell lines; of the normal purified cell populations only the monocytes were positive whereas, T, B cells, and granulocytes were negative; of primary acute (myelo) monocytic leukemia cells (CD14-positive, FAB M4/M5 morphology) 14/20 were Northern mRNA and 11/14 IEF protein positive. RT-PCR revealed MSE expression in 29/49 Northern-negative lymphoid leukemia-lymphoma cell lines. The RT-PCR signals in monocytic cell lines were on average 50-fold stronger than the mostly weak trace expression in lymphoid specimens. On treatment with various biomodulators, only all-trans retinoic acid significantly upregulated MSE message and protein levels but could not induce new MSE expression in several leukemia cell lines; lipopolysaccharide and interferon-gamma increased MSE expression in normal monocytes. Analysis of DNA methylation with sensitive restriction enzymes showed no apparent regulation of gene expression by differential methylation; the MSE gene is evolutionarily conserved among mammalian species; the half-life of the human MSE transcripts was about 5-6 h. The extent of MSE expression varied greatly among different monocytic leukemia samples. However, the MSE overexpression in a significant number of specimens was not associated with gene amplification, gross structural rearrangements or point mutations within the cDNA region. Taken together, the results suggest that MSE expression is not absolutely specific for, but strongly associated with cells of the monocytic lineage; MSE is either not expressed at all or expressed at much lower levels in cells from other lineages. The biological significance, if any, of rare MSE messages in lymphoid cells detectable only by the hypersensitive RT-PCR remains unclear. Further studies on the regulation of this gene and on the physiological function of the enzyme will no doubt be informative with respect to its striking overexpression in some malignant cells and to a possible role in the pathobiology of monocytic leukemias.
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PMID:Characterization of the monocyte-specific esterase (MSE) gene. 809 31

ICR mice were infected intranasally with Mycoplasma pulmonis isolated freshly from the lungs of the rats with pneumonia. We demonstrated with high reproducibility the expressions of messenger RNAs of cytokines, tumor necrosis factor alpha (TNF-alpha) and interferon-gamma (IFN-gamma) in the lung tissue of M. pulmonis-infected mice. Both the viable population of M. pulmonis in the lung tissue and the titers of the neutralizing antibody in the serum increased in 7 and 14 days, respectively, and reached their maxima in 35 days after infection. Macroscopical and microscopical lesions were evident in the lungs of the mice inoculated with M. pulmonis and sacrificed in 21 days after the inoculation. Microscopically, mild infiltration of mononuclear cells and neutrophils in peribronchial and perivascular spaces were observed. The alveolar septa were swollen with infiltration of these cells. Next, mRNAs prepared from the lung tissues of M. pulmonis-infected and -uninfected mice were tested for the presence of messages specific to TNF-alpha and IFN-gamma by the reverse transcriptase-polymerase chain reaction. The expression of the genes encoding TNF-alpha and IFN-gamma was constitutively demonstrated from 24h through 35 days after the intranasal inoculation of M. pulmonis. Furthermore, cells of two types, adherent and nonadherent cells, in bronchoalveolar lavage fluids obtained from the mice 3 weeks after inoculation of M. pulmonis were found also to express the genes of TNF-alpha and IFN-gamma. These data suggest that these cytokines would play a role in both stimulation and inhibition in the development of pathological changes in mycoplasmal infection, affecting the inflammatory responses.
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PMID:[Gene expression of tumor necrosis factor-alpha and interferon-gamma in the lungs of Mycoplasma pulmonis-infected mice]. 831 7

The lymphokine profiles were determined in the skin lesions of the three distinct clinical forms of American cutaneous leishmaniasis (ACL), using a reverse transcriptase polymerase chain reaction (RT-PCR) and primers for various lymphokines. The message for interferon-gamma (IFN-gamma), tumour necrosis factor-beta (TNF-beta), and IL-8 was expressed in the three clinical forms of ACL. IL-1 beta mRNA was expressed in most localized (LCL) and mucocutaneous (MCL) leishmaniasis, but in only few of the diffuse cutaneous leishmaniasis (DCL). IL-2 mRNA was detected in about half of the lesions, with more prominent values for MCL. IL-4 mRNA was present in most lesions from the three clinical forms, but markedly increased in DCL. IL-5 and IL-10 mRNAs were expressed in all MCL and in half of the DCL lesions and weakly expressed in LCL lesions. IL-10 mRNA was more abundant in MCL lesions. In contrast, IL-6 and TNF-alpha mRNAs were expressed in a large number of LCL. In MCL, IL-6 mRNA was expressed in most cases and TNF-alpha mRNA in all the cases. In DCL, IL-6 mRNA was absent and TNF-alpha mRNA was weakly expressed. These results suggest that most T cells present in the MCL and DCL lesions secrete a mixture of type 1 and type 2 cytokine patterns, but in DCL granulomas type 2 cytokines predominate. In LCL the cytokine patterns show a mixture of type 1 and type 0 with a preponderance of IFN-gamma over IL-4, and low levels of IL-5 and IL-10. The lack of IL-6 and TNF-alpha mRNAs, and the low expression of IL-1 beta in DCL lesions suggest a defect in the antigen-processing cells that may account for the state of unresponsiveness in these patients.
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PMID:Determination of the cytokine profile in American cutaneous leishmaniasis using the polymerase chain reaction. 844 70


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