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

---

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

ICR mice were infected intranasally with Mycoplasma pulmonis isolated freshly from the lungs of a rat 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 by the reverse transcriptase-polymerase chain reaction and confirmed specific mRNA of the cytokines by restriction endonuclease digestion. Both the viable population of M. pulmonis in the lung tissue and the titers of the neutralizing antibody in the serum increased between 7 and 21 days, and reached their maximum 35 days after infection. The pneumonia in mice progresses with the development of lung lesions after 7 days of infection. The early lesions are characterized primarily by neutrophils and edema in the alveolar spaces. mRNAs prepared from the lung tissue of M. pulmonis-infected and -uninfected mice were also 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 24 hr 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 also found to express the genes of TNF alpha and IFN gamma respectively. These data suggest that these cytokines would play a role in both stimulation in the development of pathological changes in mycoplasmal infection, affecting the inflammatory responses.
...
PMID:Gene expression of tumor necrosis factor alpha and interferon gamma in the lungs of Mycoplasma pulmonis-infected mice. 793 58

Constitutive expression of mRNAs for GRO alpha, GRO beta, GRO gamma, and MCP-1, belonging to the chemokine family of 8- to 10-kDa cytokines with chemotactic properties for granulocytes and monocytes, has been identified in freshly isolated human nasal and bronchial epithelium, and in bronchoalveolar macrophages (AM). Expression of GRO alpha, GRO gamma, and MCP-1, but not GRO beta, was found in airway epithelial cells. AM expressed all three GRO genes in addition to MCP-1. On reverse transcription, chemokine mRNAs yielded 0.5-30 cDNA molecules/cell, depending on the chemokine and cell type, as determined by a semiquantitative reverse transcriptase-polymerase chain reaction technique. When chemokine mRNA expression in AM and bronchial epithelium from healthy nonatopic individuals was compared, AM expressed more GRO alpha, but similar levels of GRO gamma, MCP-1, and interleukin-8 (IL-8), as in the bronchial epithelial cells. Modulation of chemokine expression by tumor necrosis factor-alpha (TNF-alpha; 10 ng/ml) or endotoxin [lipopolysaccharide (LPS), 100 ng/ml] exposure was studied in primary nasal epithelial cell and alveolar macrophage cultures. In epithelial cells, LPS did not induce chemokine expression but GRO alpha, IL-8, and MCP-1 were upregulated approximately 100-fold by TNF alpha; GRO gamma expression was elevated only 1.5- to 4-fold. In AM cultures, all three GROs were strongly induced by LPS with peak mRNA expression 24 h after stimulation (approximately 50- to 100-fold increase compared with control cultures). MCP-1 mRNA expression, on the other hand, was not increased by LPS in AM. GRO protein was present in supernatants of stimulated epithelial cells and AM.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:Constitutive and stimulated MCP-1, GRO alpha, beta, and gamma expression in human airway epithelium and bronchoalveolar macrophages. 816 97

Plasma levels of tumor necrosis factor-alpha (TNF alpha) and the ability of plasmas to induce HIV expression in chronically infected cell lines were measured in samples from adults, cord blood, and neonates from Zaire and North America. Plasma levels of TNF alpha were higher in Zairian neonates born to HIV-negative and -positive mothers than in uninfected Zairian adults (612 vs. 128 vs. 8 pg/mL, P < .001); this dichotomy persisted until children were 9 months old. Plasmas from neonates of HIV-negative Zairian mothers also stimulated higher levels of reverse transcriptase from HIV-infected cell lines than did plasma from HIV-negative Zairian adults (1339 vs. 110 cpm, P < .001). Similar patterns were noted in plasmas from HIV-negative North American adults and neonates; however, TNF alpha levels were markedly lower, and smaller differences were noted among North American adults and neonates than those in the Zairian cohort. Markedly elevated plasma TNF alpha levels in Zairian neonates and infants may play a role in the pathogenesis and progression of HIV disease in this patient population.
...
PMID:Elevated levels of tumor necrosis factor-alpha in Zairian neonate plasmas: implications for perinatal infection with the human immunodeficiency virus. 816 28

The observations of 2 types of CD4+ T cells (Th1 and Th2), which can be distinguished by their different cytokine profiles, has led to the possibility that analysis of cytokine profiles produced locally within transplanted allografts could be predictive of rejection or acceptance of that graft. We have investigated the expression of IL-2 and TNF beta (Th1 type cytokines), IL-4 and IL-10 (Th2 type cytokines), and the proinflammatory cytokines TNF alpha and IL-1 beta in sequential endomyocardial biopsies collected from 12 cardiac transplant recipients during the first 4 months after transplantation, by the analysis of RNA extracted from each biopsy by reverse transcriptase-polymerase chain reaction. The results obtained were compared with histopathological and clinical indicators of rejection. IL-2 was found in all severe (grade 3), in 57% of moderate (grade 2), in 21% of mild (grade 1) rejection, and in only 1 nonrejection (subsequently progressing to grade 3), where rejection was classified by routine histology. IL-4 and IL-10 were absent from grade 3 rejection, but present in 24% (IL-4) and in 17% (IL-10) of mild rejection and in a single nonrejecting biopsy, respectively. IL-4 was found in 2 cases of moderate rejection, and IL-10 in 1 case of moderate rejection. Statistical analysis showed that the presence of IL-2 positively correlated with both mild and moderate rejection, while IL-4 correlated with mild rejection (P < or = 0.05). IL-1 beta, TNF alpha, and TNF beta were found in both rejecting and nonrejecting biopsies, with no significant differences between the histological grades. Our results suggest that in the human situation, IL-2 and IL-4 may indeed be important in the modulation of rejection.
...
PMID:Local production of cytokines in the human cardiac allograft. A sequential study. 818 71

Bone marrow (BM) and peripheral blood (PB) cells from patients with juvenile chronic myelogenous leukemia (JCML) exhibit spontaneous in vitro proliferation. Several cytokines including granulocyte-macrophage colony-stimulating factor (GM-CSF), interleukin-1 beta (IL-1 beta), and tumor necrosis factor alpha (TNF alpha) have been implicated in supporting the growth of leukemic monocyte-macrophage colonies either by autocrine or paracrine pathways. In seven untreated JCML patients, we investigated the role of IL-1 in the spontaneous growth of these cells by specifically blocking IL-1 receptors. The IL-1 receptor antagonist (IL-1 Ra) was added to the clonogenic assays, and in each case significant (mean = 63%, range = 35% to 82%) inhibition of spontaneous proliferation was observed. Uncultured circulating cells from PB or BM of four out of five patients expressed IL-1 beta-specific mRNA and secreted the protein into the culture supernatants. Moreover, by means of reverse transcriptase-polymerase chain reaction (RT-PCR), we demonstrated that most of the spontaneously growing leukemic colony-forming unit cells (CFU-C) obtained from BM cells of two patients were positive for the presence of the IL-1 beta-specific mRNA. Despite the presence of a measurable amount of GM-CSF in JCML cell culture supernatants, GM-CSF-specific mRNA in CFU-C cells of four cases was not detected by RT-PCR. These data further support a central role for IL-1 beta in the pathogenesis of JCML and suggest that the use of IL-1 Ra could represent a novel therapeutic strategy against this disorder.
...
PMID:Suppression of juvenile chronic myelogenous leukemia colony growth by interleukin-1 receptor antagonist. 794 96

In previous studies we showed that cultured human keratinocytes expressed the 55-kD TNF receptor (TNFR) and that its expression the important for TNF alpha-mediated upregulation of intercellular adhesion molecule-1 (ICAM-1) expression on keratinocytes. Because factors that either reduce or enhance TNFR expression are likely to have a major impact on the biological effects of TNF alpha on keratinocytes, these studies were conducted to determine the factors that regulate its expression on keratinocytes. Using reverse transcriptase polymerase chain reaction, human keratinocytes were shown to lack 75-kD TNFR expression, indicating that TNF responsiveness of human keratinocytes critically depended on regulation of 55-kD TNFR expression. Human keratinocyte 55-kD TNFR surface and mRNA expression was found to be regulated in vitro by recombinant human (rh) TNF alpha. Stimulation of keratinocytes with rhTNF alpha initially decreased, but later increased, 55-kD TNFR surface expression. This biphasic modulation of 55-kD TNFR surface expression was associated with concomitant changes in 55-kD TNFR mRNA expression. Ultraviolet B (UVB) radiation, a well-known inducer of synthesis and secretion of TNF alpha by human keratinocytes, was found to mimic TNF alpha-induced modulation of 55-kD TNFR surface and mRNA expression via a TNF alpha-mediated autocrine regulatory mechanism. Production of soluble 55-kD TNFR by human keratinocytes remained unaffected by TNF alpha stimulation or UVB irradiation. These studies provide clear evidence that membrane expression of the human 55-kD TNFR may be regulated in human keratinocytes by the ligand itself: TNF alpha. Since in previous studies UVB irradiation transiently inhibited TNF alpha-induced human keratinocyte ICAM-1 expression, it is proposed that UVB radiation-induced biphasic modulation of human keratinocyte 55-kD TNFR expression may affect the capacity of these cells to respond to TNF alpha.
...
PMID:The 55-kD tumor necrosis factor receptor on human keratinocytes is regulated by tumor necrosis factor-alpha and by ultraviolet B radiation. 839 91

Langerhans cells (LC) are Ag-presenting cells required for induction of primary immune responses in skin. After activation by Ag, LC express increased levels of MHC class II Ag, exhibit increased accessory cell activity, and migrate to regional lymph nodes where they stimulate T cells. One of the earliest manifestations of LC activation is the accumulation of increased amounts of IL-1 beta mRNA in LC within 15 min after exposure to contact allergens in vivo. To determine if enhanced IL-1 beta production by LC could be causally linked to epicutaneous sensitization, we injected IL-1 beta intradermally into the ears of BALB/c mice and extracted total epidermal RNA 4 h later. A quantitative reverse transcriptase-polymerase chain reaction technique was used to compare changes in IL-1 alpha, IL-1 beta, macrophage inflammatory protein 2, IL-10, TNF-alpha, and 1-A alpha chain mRNA signals caused by intradermally-injected IL-1 beta to those caused by intradermal IL-1 alpha or TNF alpha, or by topical application of the contact allergen trinitrochlorobenzene (3% TNCB). Intradermal injection of 25 ng IL-1 beta resulted in 5-to 100-fold enhancement of mRNA signals for IL-1 alpha, IL-1 beta, MIP-2, IL-10, TNF alpha, and class II I-A alpha, mimicking the changes caused by allergen. In contrast, injection of equivalent amounts of IL-1 alpha or TNF alpha did not significantly alter the epidermal cytokine pattern. Simulating the effects of topically applied TNCB, intradermally-injected IL-1 beta (but not IL-1 alpha or TNF alpha) also caused enhancement of LC MHC class II expression. In addition, LC derived from IL-1 beta-injected skin were 2 to 3 times more potent accessory cells in an anti-CD3 proliferation assay than LC from IL-1 alpha or sham-injected skin. Finally, injection of hamster anti-mIL-1 beta mAb into the skin prior to TNCB treatment completely prevented sensitization to this allergen, although injections of similar amounts of hamster anti-mIL-1 alpha mAb or PBS were without effect. Taken together, our data indicate that dendritic cell-derived IL-1 beta may be a critical molecule required for initiation of primary immune responses in skin.
...
PMID:An essential role for Langerhans cell-derived IL-1 beta in the initiation of primary immune responses in skin. 847 27

Tumor necrosis factor-alpha (TNF alpha) is postulated to be a mediator of the systemic complications associated with acute pancreatitis. Neutralization of TNF alpha with monoclonal antibody ameliorates the morbidity and mortality associated with acute pancreatitis in a rat model. Although high levels of TNF alpha are measurable in peripheral blood in acute pancreatitis, specific sites of TNF alpha production in this disease have not been described. In this study we show that induction of pancreatitis causes up-regulation of TNF alpha messenger RNA (mRNA) at a distant organ site, the spleen. Hemisplenectomies were performed in male Sprague-Dawley rats prior to induction of pancreatitis by pancreatic duct infusion of artificial bile. Completion hemisplenectomies were then performed at 30 min, 1 hr, and 2 hr after pancreatitis induction. Quantitation of TNF alpha mRNA in the hemispleens before and after pancreatitis using a semiquantitative reverse transcriptase-polymerase chain reaction method revealed an 80-fold increase in amount of TNF alpha mRNA by 2 hr after induction of pancreatitis. By contrast, control rats receiving a sham operation showed no significant increase in TNF alpha mRNA expression after infusion of the pancreatic duct with saline. The increase in TNF alpha mRNA production was associated with increased serum TNF alpha product levels and was independent of endotoxin. We conclude that severe acute pancreatitis in the rat model is associated with significant up-regulation of TNF alpha mRNA in splenic mononuclear cells. These data provide evidence that the local events of acute pancreatitis can induce up-regulation of TNF alpha mRNA at a distant site and suggest a possible mechanism of pathogenesis of the systemic manifestations of this disease.
...
PMID:Up-regulation of TNF alpha mRNA in the rat spleen following induction of acute pancreatitis. 853 66

There is considerable evidence to suggest that polypeptide growth factors from either the oviduct or the endometrium can control preimplantation development of the mammalian embryo. These act directly through receptors expressed on the embryo. In addition, embryos also produce growth factors. The reverse transcriptase-polymerase chain reaction (RT-PCR) was used to determine the pattern of expression of mRNAs encoding several growth factor ligand and receptor genes throughout preimplantation development of cryopreserved human embryos. Transcripts encoding the receptor for c-fms, the receptor for colony-stimulating factor-1 (CSF-1), and c-kit (the receptor for stem cell factor [SCF]) were expressed throughout preimplantation development. Other growth factor ligand and receptor transcripts were expressed in a stage-specific manner: these included receptors for interleukin (IL)-6 (IL-6R), leukemia inhibitory factor (LIFR), tumor necrosis factor alpha (TNF alpha) (TNFRp80 and TNFRp60), and gp130. The transcripts for gp130 and the ligand SCF showed stage-specific splice variants. Blastocysts expressed a novel cDNA encoding gp130, which predicts a truncated form lacking the intracellular signaling domain. No expression of mRNAs encoding LIF, CSF-1, or the cloned receptor for platelet-activating factor was seen in any embryonic stage studied. We have shown that RT-PCR provides a sensitive and powerful method for identifying transcripts encoding growth factors and their receptors in single human embryos. The method is economical, allowing the expression pattern of many genes to be determined from a single embryo. These data are important in defining which cytokines may be involved in regulating human preimplantation development and when they may act.
...
PMID:Stage-specific expression of cytokine and receptor messenger ribonucleic acids in human preimplantation embryos. 854 94

Polypeptide 48 is a 48,000 MW protein, originally isolated from conditioned media of some human leukaemic cell lines, that induces differentiation and cytolytic activity in HL-60 promyelocytic leukaemia cells and activates human peripheral blood monocytes to secrete interleukin-1 (IL-1) and tumour necrosis factor-alpha (TNF-alpha). In the present study we examined the effects of p48 on the accumulation of a series of monokine transcripts, including TNF-alpha, IL-1 alpha, IL-1 beta and IL-6, in human peripheral blood monocytes and the myeloid/monocyte cell lines HL-60 and U937. Using reverse transcriptase polymerase chain reaction (RT-PCR) and Northern blot analysis, p48 was found to induce accumulation of TNF-alpha, IL-1 alpha and IL-1 beta mRNA in peripheral blood monocytes, HL-60 and U937 cells. IL-6 mRNA was found to be increased in p48-stimulated peripheral blood monocytes but not HL-60 or U937. Thus, the secretion of IL-1 and TNF-alpha by p48-stimulated monocytic cells was associated with up-regulation of cytokine mRNA, suggesting that p48 leads to increased transcription or mRNA stability in these cells. As U937 and HL-60 are likely to represent premonocyte stages of haemopoietic differentiation, it is possible that the effect of p48 on IL-6 mRNA, in contrast to its effect on TNF and IL-1, requires cells to be at a later differentiation step.
...
PMID:Up-regulation of cytokine mRNA in human monocytes and myeloid cell lines by the differentiation/activation factor p48. 855 86


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>

---