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)

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

Trehalose dimycolate (TDM), a glycolipid present in the cell wall of Mycobacterium spp., is a powerful immunostimulant. TDM primes murine macrophages (Mphi) to produce nitric oxide (NO) and to develop antitumoral activity upon activation with low doses of lipopolysaccharide (LPS). In this study, we investigated the ability of TDM to induce interleukin 12 (IL-12) and the role of this cytokine in TDM-induced activation of murine Mphi. RNA isolated from peritoneal exudate cells (PEC) collected at different times after TDM injection was used to determine IL-12 (p35 and p40 subunits) and gamma interferon (IFN-gamma) mRNA levels by semiquantitative reverse transcriptase-PCR. Constitutive expression of IL-12p35 was observed in PEC from untreated as well as from TDM-injected mice. In contrast, expression of the IL-12p40 subunit was almost undetectable in control PEC but was dramatically upregulated in PEC from TDM-injected mice. IL-12p40 expression peaked at 8 h and subsided to baseline levels at 39 h postinjection. TDM was also able to induce IFN-gamma expression; however, kinetics of induction of IFN-gamma was different from that of IL-12p40. Maximal levels of IFN-gamma mRNA were reached by 24 h and did not return to baseline by 4 days. In addition, pretreatment of mice with neutralizing monoclonal antibodies directed against IL-12 (C15.6.7 and C15.1.2) blocked IFN-gamma mRNA induction in PEC from TDM-treated mice. We further determined if the induction of IL-12 and/or IFN-gamma contributes to the in vivo priming effect of TDM on peritoneal Mphi. TDM-injected mice were treated in vivo with anti-IL-12 or anti-IFN-gamma (XMG.1.6) monoclonal antibodies. TDM-primed Mphi were then activated in vitro with LPS and tested for their ability to produce NO and to develop cytostatic activity toward cocultivated L1210 tumor cells. Priming of Mphi by TDM was completely blocked by in vivo neutralization of either IL-12 or IFN-gamma as demonstrated by an absence of tumoricidal activity and NO production by TDM-elicited Mphi in the presence of LPS. Taken together our results show that TDM, a defined molecule from M. tuberculosis, induces in vivo production of IL-12. Moreover, synthesis of IL-12 mediates TDM priming of mouse peritoneal Mphi through IFN-gamma induction.
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PMID:Interleukin-12 synthesis is a required step in trehalose dimycolate-induced activation of mouse peritoneal macrophages. 911 75

The small bowel has a unique amount of closely associated lymphoid tissue in the form of mesenteric lymph nodes (MLNs) and Peyer's patches (PPs). It is rather unclear how this may affect the immune response to transplants involving small bowel. It is clear, however, that host-derived leukocytes infiltrate this lymphoid tissue very rapidly after transplantation of small bowel, which suggests the possibility of an early immune response within this compartment. To investigate this possibility, we analyzed, using a semiquantitative reverse transcriptase-polymerase chain reaction, the level of cytokine transcripts within isolated MLNs and PPs for the first 7 days after small bowel transplantation. Heterotopic small bowel (n=32) transplants were performed using the following rat strain combinations: syngeneic Lewis (Lew)-->Lew (n=8), blood group D Agouti (DA)-->DA (n=8), allogeneic Lew-->DA (n=8), and allogeneic DA-->Lew (n=8). Two rats from each group were killed at 1, 3, 5, and 7 days after transplantation. RNA was prepared separately from PPs and MLNs before analysis of transcripts for interleukin (IL) 2, IL-4, IL-10, IL-6, IL-1alpha, and interferon (IFN) gamma. No increase in transcripts for IL-2 or IL-10 was observed in either PPs or MLNs of syngeneic grafts. A small rise in IL-6, IL-1alpha, and IFN-gamma transcripts was seen in MLNs and IFN-gamma transcripts in PPs of syngeneic grafts. In contrast, in allografts an extremely early increase in cytokine transcripts was observed; all cytokine transcripts tested were elevated within the first 24 hr after transplantation. Indeed, the peak response of both IL-2 and IL-10 occurred within 1 to 3 days after grafting. This early immune response in the lymphoid tissue may not be controlled by immunosuppression delivered only at the time of transplantation, and therefore may be responsible for the difficulty in achieving adequate immunosuppression in small bowel transplantation.
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PMID:The immune response following small bowel transplantation. II. A very early cytokine response in the gut-associated lymphoid tissue. 913 73

Numerous cytokines induce symptoms characteristic of the flu syndrome common to acute viral infections. To better characterize the cytokine mRNA profile associated with the early phase of this syndrome, we examined the induction of cytokine mRNAs in spleens of mice 1, 2, and 4 h following intraperitoneal inoculation of Newcastle disease virus (NDV). The reverse transcriptase-polymerase chain reaction was used to detect mRNAs for mouse proinflammatory cytokines [interleukin (IL)-1 alpha, IL-1 beta, IL-6, tumor necrosis factor-alpha (TNF-alpha), macrophage colony-stimulating factor (M-CSF), and interferon (IFN)-gamma] and type I IFNs (IFN-alpha 4 and IFN-beta). We observed a rapid (within 2 h) induction of most of these cytokine mRNAs in the mouse spleen following challenge with live NDV or the viral stimulant poly[rI:rC]. IL-1 beta, M-CSF, and IFN-gamma mRNAs were also induced by heat-inactivated NDV, suggesting the possibility of endotoxin contamination of the virus (confirmed by Limulus lysate assay). Examination of cytokine induction by comparable doses of lipopolysaccharide indicated that endotoxin contamination could account for the cytokine mRNA-inducing activity of the heat-inactivated virus. These studies point to a critical control (heat-inactivated virus) for viral cytokine studies. In addition, they indicate that certain cytokine mRNAs (IL-1 alpha, IL-6, M-CSF, IFN-gamma, IFN-alpha, and IFN-beta) are rapidly induced in the spleen when live virus is inoculated intraperitoneally, independently of contaminating endotoxin.
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PMID:Early induction of proinflammatory cytokine and type I interferon mRNAs following Newcastle disease virus, poly [rI:rC], or low-dose LPS challenge of the mouse. 914 48

This article explores the clinical usefulness of reverse transcriptase-polymerase chain reaction in organ graft recipients. In this study, reverse transcriptase-polymerase chain reaction was used to identify intrarenal expression of cytotoxic attack molecules (granzyme B and perforin) and immunoregulatory cytokines (IL-2, IL-4, IL-10, IFN-gamma, and TGF-beta 1) in human renal allograft biopsies. The biopsies (n = 127) were classified using the Banff criteria, and intrarenal gene expression was correlated with the histologic diagnosis. Molecular analyses revealed that intragraft display of mRNA encoding granzyme B, IL-10, or IL-2 is a correlate of acute rejection, and intrarenal expression of TGF beta 1 mRNA is a correlate of chronic rejection. In addition to demonstrating differential and highly selective intragraft gene expression during rejection, these data suggest that therapeutic strategies directed at the molecular correlates of rejection might refine existing antirejection strategies.
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PMID:Clinical application of molecular biology: a study of allograft rejection with polymerase chain reaction. 914 34

Cytokine gene expression was examined by qualitative and semiquantitative reverse transcriptase polymerase chain reaction (RT-PCR) in the lungs of Mycoplasma pneumoniae infected immune C57BL/6 mice depleted of either CD4+, CD8+ or both CD4+ and CD8+ T cells. Immediately after M. pneumoniae reinfection of control immune mice, mRNAs for TNF-alpha, IFN-gamma, IL-1 beta, IL-6, IL-2 and IL-2 receptor were promptly detected in the lungs. In animals depleted of CD4+ T cells, mRNA expression for IL-2, IL-2 receptor and IFN-gamma were completely abrogated and mRNA expression for TNF-alpha, IL-1 beta and IL-6 were reduced by 10- to 100-fold. In mice depleted of CD8+ T cells, mRNA expression for IL-2 and the IL-2 receptor was also undetectable, while mRNA for TNF-alpha, IL-1 beta and IL-6 were only marginally decreased. Histological evaluation of the infected lungs performed in parallel revealed dense mononuclear infiltrations around small bronchi and small blood vessels in control reinfected mice. In contrast, in CD4+ T cell-depleted mice, these focal accumulation of lung tissue infiltrating cells were found to be greatly reduced. The data indicate that the inflammatory response in lung tissue thought to be mainly responsible for Mycoplasma pneumoniae disease is associated with an increased level and a prolonged expression of proinflammatory cytokines due to CD4+ lung infiltrating T cells.
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PMID:Cytokine gene expression in immune mice reinfected with Mycoplasma pneumoniae: the role of T cell subsets in aggravating the inflammatory response. 914 34

NK1.1+ CD4+ T cells produce IL-4 promptly in vivo upon injection of anti-CD3 and may play a role in initiating Th2 cell-mediated immunity. To characterize their in vitro activation properties, NK1.1+ CD4+ T cells were obtained in high purity from spleens of normal C57BL/6 mice, where they represent 2 to 5% of CD4+ T cells, or from MHC-class II I-Ab gene knockout mice, where they constitute 42% of CD4+ T cells. Activation of NK1.1+ CD4+ T cells from either source with plate-bound anti-CD3 resulted in loss of expression of NK1.1 as determined both by flow cytometric analysis and by reverse transcriptase-PCR analysis. A portion of these cells also lost CD4 expression. Both the CD4+ and CD4- activated cells retained the over-representation of V beta8 and V alpha14 chains and expressed the intermediate levels of the TCR-CD3 complex that is characteristic of resting NK1.1+ CD4+ T cells. The anti-NK1.1 mAb used for cell sorting was not the cause of NK1.1 or CD4 disappearance, since the sorted cells remain both NK1.1+ and CD4+ when cultured in the absence of anti-CD3 or in the presence of anti-CD3 and cyclosporin A. Furthermore, NK1.1+ CD4+ T cells that were not treated with anti-NK1.1 Ab also lost NK1.1 expression after activation. Populations of activated CD4+ and CD4- cells (derived from NK1.1+ CD4+ T cells) produced both IL-4 and IFN-gamma upon restimulation with plate-bound anti-CD3.
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PMID:NK1.1+ CD4+ T cells lose NK1.1 expression upon in vitro activation. 916 26

Rhesus macaques were orally immunized with a mucosal vaccine consisting of two different concentrations (1 mg vs 250 microg) of recombinant SIV p55gag (p55) with or without cholera toxin (CT, 50 microg) as a mucosal adjuvant. The plasma from macaques receiving the higher dose of p55 (1 mg) and CT had higher p55-specific IgG and IgA Ab titers compared with macaques that received the lower dose of p55 (250 microg) and CT. Further, high levels of p55-specific IgG and IgA Abs were present in external secretions from both groups. The level of p55-induced T cell responses was elevated in PBMCs isolated from the high dose group compared with the low dose group. When culture supernatants from these p55-stimulated PBMCs were examined for Th1 (IFN-gamma) and Th2 (IL-4 and IL-10) cytokines, both IFN-gamma and IL-10 were present, but IL-4 was absent. CD4+ T cells isolated from these p55-stimulated PBMCs contained IFN-gamma spot-forming cells (SFCs) but not IL-4 SFCs. These results were further confirmed by cytokine-specific reverse transcriptase PCR analysis, where p55-specific CD4+ T cells expressed mRNA for IFN-gamma, IL-6, and IL-10, but not IL-4. These findings suggest that oral immunization of nonhuman primates induced both IFN-gamma-secreting Th1 and select Th2 cytokine (e.g., IL-6 and IL-10)-producing CD4+ Th cells, which accounted for the generation of p55-specific systemic and mucosal Ab responses.
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PMID:Oral immunization with simian immunodeficiency virus p55gag and cholera toxin elicits both mucosal IgA and systemic IgG immune responses in nonhuman primates. 916 52

We have used a semi-quantitative reverse transcriptase-polymerase chain reaction (RT-PCR) assay to detect the expression of mRNA for inflammatory cytokines, integrins and selectins in murine lung tissue, and T cells and eosinophils isolated from lung and bronchoalveolar lavage (BAL) fluid in an in vivo model of ovalbumin (OA)-induced airway inflammation. RNA was isolated from whole lung tissue at 1, 6, 24, 48, 72 h, and 7 days after OA inhalation. mRNA for the Th2 cytokines, IL-4, -5, -6, -10 and -13 in OA-sensitized mice were significantly elevated compared with non-sensitized mice. IL-2, TNF-beta, and eotaxin mRNA were also increased, but IFN-gamma mRNA was not. P- and E-selectin mRNA levels were also enhanced in lung tissue between 6 and 72 h after challenge. Lung T cells were isolated by cell sorting with a flow cytometer at 3, 12, 24, 48 and 72 h after challenge. mRNA levels for IL-5 and -10 were greater in T cells from OA-sensitized and -challenged mice than controls at 24 h. BAL fluid from OA-sensitized and -challenged mice also had significantly higher IL-5 levels than controls. BAL fluid T cells and eosinophils were obtained at 48 and 72 h after aerosol challenge and were purified by cell sorting. Messenger RNA for IL-1 alpha, -2, -4, -5, -10, IFN-gamma, and beta 1 were detected in T cells at both time points. Transcripts for IL-1 alpha, -4, -5, -13, TNF-alpha and beta, and alpha 4, beta 1 and beta 7 were also identified in BAL eosinophils. These data show that in addition to murine lung T cells, airway eosinophils may also contribute to the inflammatory response by their ability to express mRNA for cytokines and integrins.
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PMID:Identification of cytokine and adhesion molecule mRNA in murine lung tissue and isolated T cells and eosinophils by semi-quantitative reverse transcriptase-polymerase chain reaction. 919 71

Acute oral exposure of B6C3F1 mice to vomitoxin (VT) has been previously shown to induce expression of mRNAs for cytokines that are characteristically produced in lymphoid tissues by macrophage and T cells. The purpose of this study was to evaluate the effects of VT dose on the expression of mRNAs for a cytokine profile consisting of TNF-alpha, IL-1beta, IL-6, IL-12, IFN-gamma, IL-2, IL-4, IL-5, IL-10, IL-12, and TGF-beta and to measure the kinetics of these responses. The effects of a single oral exposure to 0, 0.1, 0.5, 1, 5, and 25 mg/kg BW of VT on cytokine mRNA abundance in spleen and Peyer's patches (indicators of systemic and mucosal immune compartments, respectively) were assessed at 2 hr postexposure using reverse transcriptase-polymerase chain reaction (RT-PCR) in combination with hybridization analysis. Both 5 and 25 mg/kg VT significantly induced the mRNAs for the proinflammatory cytokines IL-1beta, IL-6, and TNF-alpha; the T helper 1 cytokines IFN-gamma and IL-2; and the T helper 2 cytokines IL-4 and IL-10, whereas lower doses had no effect. IL-12p40 mRNA was also induced but not IL-12p35 mRNA. The effects were more pronounced in spleen than in the Peyer's patches. IL-5 and TGF-beta mRNAs were expressed constitutively in spleen and Peyer's patches but were not affected by VT. When cytokine mRNA levels were measured at 1, 2, 4, 8, and 24 hr after oral exposure to 25 mg/kg BW of VT, mRNA expression kinetics varied among cytokines or between spleen and Peyer's patches. The duration of elevated mRNA expression in spleen was 1-8 hr for TNF-alpha, IL-6, IFN-gamma, and IL-10 and was 1-4 hr for IL-1beta, IL-12p40, IL-2, and IL-4. In Peyer's patches, duration periods were 1-8 hr for IL-6, IL-2, and IL-10; 1-4 hr for IL-1beta, IL-12p40, and TNF-alpha; and 1-2 hr for IFN-gamma. Serum levels of TNF-alpha, IL-6, and IFN-gamma were elevated 3 hr after exposure to 25 mg/kg VT, thus suggesting that elevation of splenic and Peyer's patch mRNA abundance correlated with increases in systemic production of these cytokines. Taken together, the results indicate that a single VT exposure rapidly induces gene expression in vivo for a wide range of cytokines with apparently complete recovery occurring after 24 hr. Elevated cytokine expression may play an important role in the pathophysiologic effects of VT and other trichothecenes.
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PMID:Differential cytokine mRNA expression in mice after oral exposure to the trichothecene vomitoxin (deoxynivalenol): dose response and time course. 919 13


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