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)

Lymphoma was diagnosed in a 7-year-old domestic cat found to be infected with FeLV and feline immunodeficiency virus (FIV). The cat was affected by chronic disorders suggestive of immunosuppression, including gingivitis, periodontitis, keratitis, and abscesses. Despite treatment, peripheral keratitis of the left eye progressed, resulting in uveitis, chronic glaucoma, and eventual corneal rupture. Microscopic retinal and optic disk pathologic processes also were suspected. Abnormal jaw movements that were believed to be indicative of neurologic disease were observed. Approximately 17 months later, the cat developed generalized lymphadenopathy, hepatosplenomegaly, and bilateral renomegaly. Lymphoblastic lymphoma and glomerulonephritis were diagnosed histologically. Manganese- and magnesium-dependent reverse transcriptase activity were detected in supernatants from lymph node and spleen mononuclear cell cultures, suggesting T-lymphocyte infection with FeLV and FIV.
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PMID:Feline leukemia virus and feline immunodeficiency virus infections in a cat with lymphoma. 253 74

We have shown that gamma delta T cells in human gingiva have an intraepithelial location and, that in the chronic inflammatory disease periodontitis, the expression of CD45RO and CD8 or CD4 is induced on gamma delta T cells. To study the role of gamma delta T cells in local antibacterial responses, we determined the cytokine profiles of isolated human gingival cells. Different T cell subpopulations, isolated by positive selection with mAb-coated magnetic beads and macrophages, as well as epithelial cells, were analyzed for expression of mRNA for 15 cytokines by reverse transcriptase-PCR. The ultrastructure of gingival gamma delta T cells was also studied. The gamma delta T cells expressed mRNA for IFN-gamma, TNF-alpha, TGF-beta 1, and IL-6. Expression of IFN-gamma was a consequence of inflammation. CD4+ gamma delta T cells expressed IFN-gamma only, whereas CD8+ gamma delta T cells expressed all four cytokines. CD8+ cells expressing IFN-gamma, TNF-alpha, and IL-6 in combination suggest a cytotoxic effector function. Gingival gamma delta T cells contained cytoplasmic electron-dense membrane-bound granules and multivesicular bodies that are ultrastructural characteristics of cytotoxic cells. Epithelial cells from inflamed gingiva expressed HLA-DR, CD1a, CD1c, and heat shock protein 60 on the cell surface. They also expressed mRNA for IL-1 beta, IL-6, IL-8, TNF-alpha, and TGF-beta 1. Thus, epithelial cells may function as accessory cells in immune activation and, at the same time, be target cells for CD8+ gamma delta T cells reactive with CD1 Ag or heat shock protein. These results suggest that gamma delta T cells constitute a first line of defense in gingiva, preventing entrance of pathogens by cytotoxicity against infected and stressed epithelial cells, and by control of epithelial cell growth through secretion of regulatory cytokines.
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PMID:Cytokine profile and ultrastructure of intraepithelial gamma delta T cells in chronically inflamed human gingiva suggest a cytotoxic effector function. 805 26

Elevated numbers of plasma cells are associated with localized and chronically inflamed gingiva of patients with adult periodontitis. However, only limited information is currently available as to how cytokines produced by CD4(+) T cells are involved in these increased B cell responses in affected gingival tissues. When gingival mononuclear cells (GMC) were isolated from inflamed tissues and examined by flow cytometry, approximately 20-30% of lymphocytes were CD4(+) T cells. For the analysis of Th1 and Th2 cytokine expression by these CD4(+) T cells, RNA was extracted and reverse transcriptase-polymerase chain reaction (RT-PCR) was performed by using specific 5' and 3' primers for interferon-gamma (IFN-gamma) and IL-2 (Th1), IL-4, IL-5, IL-6, IL-10 and IL-13 (Th2) and beta-actin (internal control). Two distinct cytokine profiles were noted based on the expression of selected Th1 and Th2 cytokines, where one pattern was represented by expression of mRNA for IFN-gamma, IL-6, IL-10 and IL-13, while the second consisted of mRNA for IFN-gamma, IL-6 and IL-13. In most samples, mRNA for IL-2, IL-4 and IL-5 were not detected by cytokine-specific RT-PCR. When RNA was isolated from CD4(+) T cells of concanavalin A-stimulated peripheral blood mononuclear cells (PBMC) of the same patients and examined by RT-PCR, mRNA for all Th1 and Th2 cytokines were detected. These findings suggest that although human CD4(+) T cells are capable of producing an array of Th1- and Th2-type cytokines, the CD4(+) T cells associated with periodontitis are limited to production of IFN-gamma, IL-6, IL-13 and is some instances IL-10. CD4(+) T cells from diseased periodontal tissues are divisible into two groups based upon whether or not IL-10 is produced, together with IFN-gamma, IL-6 and IL-13.
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PMID:Selected Th1 and Th2 cytokine mRNA expression by CD4(+) T cells isolated from inflamed human gingival tissues. 860 41

An accumulation of elevated numbers of macrophages (M phi) and Ig producing cells is associated with localized and chronically inflamed gingiva of patients with adult periodontitis. When gingival lymphocytes were isolated from inflamed tissues and examined by flow cytometry, approximately 20-30% of lymphocytes were CD4+ T cells. For the analysis of Th1 and Th2 cytokine expression by these CD4+ T cells, RNA was extracted and reverse transcriptase polymerase chain reaction (RT-PCR) was performed by using specific 5' and 3' primers for IFN-gamma and IL-2 (Th1), IL-4, IL-5, IL-6, IL-10 and IL-13, (Th2) and beta-actin (housekeeping gene). Two distinct cytokine profiles were noted based on the expression of selected Th1 and Th2 cytokines. Thus, one pattern was represented by the expression of mRNA for IFN-gamma, IL-6, IL-10 and IL-13, while the other case consisted of mRNA for IFN-gamma, IL-6, and IL-13. Except for a few cases, messages for IL-2, IL-4 and IL-5 were not detected by cytokine-specific RT-PCR. The predominant expression of Th2 cytokines (e.g. IL-6, IL-10 and IL-13) may contribute to the induction of high B cell responses in local disease sites. On the other hand, lack of IL-4 may be responsible for the accumulation of M phi in diseased periodontium. We also investigated whether a relationship exists between IL-4 receptor (IL-4R) expression and M phi persistence in the absence of exogenous IL-4. Gingival M phi, when compared with monocytes (MN)/M phi from peripheral blood mononuclear cells (PBMC), expressed high levels of IL-4R mRNA. When gingival M phi were incubated with recombinant IL-4 (rIL-4), the cell viability was dramatically reduced by apoptosis. These findings clearly show that the lack of IL-4 may contribute to the persistent occurrence of M phi at the disease site and addition of exogenous rIL-4 to gingival M phi cultures leads to cell death by apoptosis.
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PMID:Molecular and cellular mechanisms for periodontal diseases: role of Th1 and Th2 type cytokines in induction of mucosal inflammation. 908 20

In an attempt to clarify the immunobiological events featuring periodontitis lesions of AIDS patients in the late stage of the disease, peripheral blood (PB) and gingival crevicular fluid (GCF) leucocytes from periodontitis lesions of 23 late-stage AIDS patients were analysed by three-colour flow cytometry for detection and identification of intracytoplasmic p24+ cell fractions. The cells were reacted with CD14 and CD68 for mononuclear phagocytes or with CD4 and CD14 for Th cells, then with anti-p24 MoAb. To detect HIV proviral sequences and intracellular p24 RNA sequences, genomic DNA and cellular RNA from leucocytes were extracted for semi-nested polymerase chain reaction (PCR) amplification. CD68+/p24+ and CD14+/CD68+/p24+ fractions were larger in GCF than in PB (P<0.0001; P < 0.003). CD14+/p24+ fraction was lower in GCF than in PB (P < 0.05). The fluorescence intensities (FI) for intracellular p24 in CD68+ and CD14+/CD68+ cells were higher in GCF than in PB (P < 0.003; P < 0.02), whereas those of CD14+ macrophages did not differ. The p24 FI of CD68+ macrophages in GCF correlated with CD4+ lymphocyte counts in PB (P < 0.005). p24 FI levels of CD14+ monocytes in GCF and PB significantly correlated (P < 0.02), whereas that of CD68+ macrophages did not. PCR and reverse transcriptase (RT)-PCR of cellular DNA and RNA yielded positive signals, demonstrating viral integration and production in GCF leucocytes. These results show that periodontitis lesions in AIDS patients can be characterized by a rapid macrophage turnover, and these HIV-infected macrophage exudates in GCF may be considered as a within-mouth source of virus.
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PMID:Characterization of HIV-related periodontitis in AIDS patients: HIV-infected macrophage exudate in gingival crevicular fluid as a hallmark of distinctive etiology. 915 94

Adult periodontitis is a chronic destructive disease characterized by an interaction between gram-negative bacteria and the host inflammatory response. Microbial substances such as lipopolysaccharide can activate host cells, e.g., macrophages, fibroblasts and keratinocytes, to secrete proinflammatory cytokines including tumor necrosis factor alpha and interleukin 1 beta (IL-1 beta). This study examined the hypothesis that periodontitis tissue contains increased levels of cytokines that promote osseous and connective tissue destruction. To test this hypothesis, diseased and healthy gingival biopsies were examined for differences in the expression of cytokine mRNA for the pro-inflammatory cytokines tumor necrosis factor alpha and IL-1 beta and the anti-inflammatory cytokine IL-1ra using quantitative reverse transcriptase polymerase chain reaction and in situ hybridization methods. The levels of tumor necrosis factor alpha and IL-1ra mRNA were shown to be significantly higher in diseased than healthy tissues. Additionally, a significantly correlated expression of IL-1 beta and IL-1ra mRNA was seen in all tissue examined. Analysis of tissue sections by immunohistochemical and in situ hybridization techniques revealed a mononuclear cell infiltrate that consisted of a higher average number of cells staining positive for tumor necrosis factor alpha mRNA, CD14, and CD3 in the diseased than healthy tissues. Although both diseased and healthy tissues expressed IL-1 beta and IL-1ra mRNA in the epithelium, the diseased tissue biopsies expressed more IL-1 beta and IL-1ra mRNA in the connective tissue. These results implicate the potential involvement of both the pro- and anti-inflammatory cytokines in the regulation of the chronic inflammatory disease adult periodontitis.
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PMID:Quantitative assessment of inflammatory cytokine gene expression in chronic adult periodontitis. 957 7

Periodontitis is the inflammatory response in periodontal tissues elicited by bacterial colonization in periodontal pockets. In this response, pocket epithelial cells are the first cells to come into contact with bacteria. To elucidate this mechanism, we determined the adherence of the periodontopathic bacterium Eikenella corrodens 1073, which has a GalNAc-sensitive lectin-like adhesin (EcLS), to a human oral epithelial carcinoma cell line (KB) and the induction of proinflammatory cytokine production in the cells following exposure to this bacterium in vitro. In the adherence assay, EcLS played a role as the adhesin of this bacterium in adherence to KB cells. In a reverse transcriptase PCR, significant interleukin-8 (IL-8) and IL-6 mRNA levels were induced in response to exposure to this bacterium. In an enzyme-linked immunosorbent assay after an 8-h bacterial exposure, the IL-8 and IL-6 protein levels were 13.5- and 8.3-fold higher than those in the nonexposed controls, respectively. These protein responses were time dependent. Interestingly, when E. corrodens was separated from KB cells by cell culture inserts, a slight stimulation of the IL-6 and IL-8 mRNA and secreted protein levels was seen. These results imply that the direct contact of E. corrodens 1073 with oral epithelial cells is not necessarily required for the stimulation of IL-6 and IL-8 secretion. We suggest that E. corrodens induces the epithelial cells to secrete proinflammatory cytokines which serve as an early signaling system to host immune and inflammatory cells in underlying connective tissues.
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PMID:Interleukin-6 (IL-6) and IL-8 are induced in human oral epithelial cells in response to exposure to periodontopathic Eikenella corrodens. 986 40

Campylobacter rectus is a periodontal pathogen with a 150-kDa protein on its cell surface. This protein forms a paracrystalline lattice, called the S-layer, surrounding the outer membrane of this gram-negative bacterium. To initiate a genetic analysis of the possible role of the S-layer in the initial interaction of C. rectus with host epithelial cells, C. rectus strains lacking the S-layer protein gene (crsA) were constructed by allelic exchange mutagenesis. Surprisingly, the lack of the S-layer had only a minor effect on the interaction of C. rectus with HEp-2 epithelial cells; CrsA(+) cells were 30 to 50% more adherent than were CrsA(-) bacteria. Since the host cell expression of cytokines appears to play an important role in the pathogenesis of periodontal diseases, the effect of the S-layer on the epithelial cell cytokine response was also examined by quantitative reverse transcriptase PCR and enzyme-linked immunosorbent assay. Although there were no changes in the mRNA levels for the anti-inflammatory cytokines interleukin-1 receptor agonist (IL-1ra), IL-13, and transforming growth factor beta, the expression and secretion of the proinflammatory cytokines IL-6, IL-8, and tumor necrosis factor alpha (TNF-alpha) were significantly induced by both wild-type C. rectus and CrsA(-) bacteria. Interestingly, the kinetics of cytokine induction differed for the CrsA(+) and CrsA(-) bacteria. At early time points, the HEp-2 cells challenged with CrsA(-) bacteria produced higher levels of IL-6, IL-8, and TNF-alpha mRNA and protein than did cells challenged with CrsA(+) bacteria. We conclude that C. rectus may help initiate periodontitis by increasing the expression of proinflammatory cytokines and that the S-layer may temper this response to facilitate the survival of C. rectus at the site of infection.
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PMID:Use of defined mutants to assess the role of the Campylobacter rectus S-layer in bacterium-epithelial cell interactions. 1067 61

It has been reported that lipopolysaccharide (LPS) from periodontal pathogens can penetrate gingival tissues and stimulate the production of prostaglandin E2 (PGE2), which is known as a potent stimulator of inflammation and bone resorption. Although biostimulatory effects of low-level laser irradiation such as anti-inflammatory results have been reported, the physiological mechanism is not yet clarified. The purpose of the present study was to determine the effect of laser irradiation on PGE2 production and cyclooxygenase (COX)-1 and COX-2 gene expression in LPS-challenged human gingival fibroblast (hGF) cells in vitro. hGF cells were prepared from healthy gingival tissues and challenged with LPS, and Ga-Al-As diode laser was irradiated to the hGF cells. The amount of PGE2 released in the culture medium was measured by radioimmunoassay, and mRNA levels were analyzed by reverse transcriptase-polymerase chain reaction (RT-PCR). Irradiation with Ga-Al-As diode low-level laser significantly inhibited PGE2 production in a dose-dependent manner, which led to a reduction of COX-2 mRNA levels. In conclusion, low-level laser irradiation inhibited PGE2 by LPS in hGF cells through a reduction of COX-2 mRNA level. The findings suggest that low-level laser irradiation may be of therapeutic benefit against the aggravation of gingivitis and periodontitis by bacterial infection.
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PMID:Inhibitory effect of low-level laser irradiation on LPS-stimulated prostaglandin E2 production and cyclooxygenase-2 in human gingival fibroblasts. 1070 74

Accumulating evidence indicates that TNFalpha plays an important role in the pathogenesis of periodontitis, but the effect of TNFalpha on the degradation of the periodontal ligament is not well understood. This study used reverse transcriptase-PCR to investigate the effects of TNFalpha on matrix metalloproteinase (MMP) mRNA expression in human periodontal ligament fibroblasts. TNFalpha increased MMP-1, MMP-3 and MMP-13 mRNA levels in both a time-dependent (0-24 h) and a dose-dependent (0.1-10 ng/ml) manner. TNFalpha also increased COX-2 mRNA levels. Because elevation of COX-2 mRNA levels enhances the production of prostaglandins, we therefore investigated whether endogenous prostaglandins are involved in the MMP mRNA expression that is enhanced by TNFalpha. Pretreatment with the selective COX-2 inhibitor, NS-398, increased MMP-13 mRNA levels, while prostaglandin E2 and dibutyryl cyclic AMP decreased MMP-13 mRNA levels. Neither MMP-1 nor MMP-3 mRNA levels were affected by these chemicals. These findings indicate that prostaglandin E2 has a lowering effect on TNFalpha-enhanced MMP-13 mRNA levels, and that this effect is dependent on cAMP. Our results suggest that TNFalpha participates in periodontal ligament destruction by stimulating the production of MMPs (MMP-1, MMP-3 and MMP-13), while endogenous prostaglandin E2 has a negative feedback role in TNFalpha-enhanced MMP-13 production.
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PMID:Effects of TNFalpha and prostaglandin E2 on the expression of MMPs in human periodontal ligament fibroblasts. 1211 50


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