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)

Published reports indicate that HIV is recovered from BAL fluid of patients with AIDS who have LIP but not with other AIDS-related pulmonary disease. Our experience has been different. Ten BAL specimens from nine patients with AIDS were cultured directly in peripheral blood mononuclear cells, and all ten cultures were positive for HIV as indicated by examination of the culture supernatant by reverse transcriptase assay and enzyme immunoassay for HIV antigen. Five of the specimens were also positive for Pneumocystis carinii, and other pulmonary diagnoses included histoplasmosis, lymphoma, Kaposi's sarcoma, and aspiration pneumonia. Five additional BAL specimens were cultured after freezing at -70 degrees C, but only two were culture-positive for HIV (p = 0.022; FET). This study indicates that HIV can be recovered from the BAL fluid in most patients with AIDS, unrelated to the type of pulmonary disease. In contrast to cultures, HIV antigen was detected in the BAL fluid of only one patient, and that patient had LIP with noncaseating granulomas. Therefore, HIV culture is not useful in the diagnosis of LIP, but HIV antigen detection should be studied further. All BAL fluids should be considered potentially infectious.
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PMID:Recovery of human immunodeficiency virus and detection of p24 antigen in bronchoalveolar lavage fluid from adult patients with AIDS. 250 Mar 12

The E-series prostaglandins (PGEs) are complex lipid regulators of B lymphocyte function. They inhibit the growth of certain B lymphoma lines. We report that heterogeneity with respect to PGE-induced growth inhibition correlates with the maturation state of the B cell lines. Specifically, the pre-B cell line 70Z/3 and the immature lymphoma CH31 are extremely sensitive to PGE2. To a lesser degree, other immature lymphomas (CH33, ECH408.1 and WEHI-231) are sensitive to PGE2. More mature lymphomas (BAL-17, CH12 and CH27) and fully differentiated myelomas (J558 and MOPC-315) are insensitive to PGE2. It is unknown what subtype of PGE receptor(s) (EPs) are expressed by B lymphocytes. It is also unknown if modulation of EP receptor expression could account for the differences in the sensitivity of these B cell lines to PGE2. To investigate these issues, reverse transcriptase polymerase chain reaction, Northern blot and DNA sequencing analyses were employed to obtain a definitive EP receptor subtype profile for these B cell lines, and for normal splenic B lymphocytes. Both normal and transformed B lymphocytes express mRNA encoding EP1, EP3beta and EP4 subtypes of PGE receptors. The B lineage cells do not express EP3alpha nor EP3gamma mRNA. The B cell lines are clonal, indicating that EP1, EP3beta and EP4 mRNA are coexpressed. Surprisingly, quantitative differences in basal EP1, EP3beta and EP4 expression were not observed between B cell lines despite their differing susceptibilities to PGE-induced growth inhibition. Conversely, the polyclonal activator LPS selectively upregulates EP4 mRNA expression in the mature B cell line CH12, but not in the LPS-sensitive pre-B cell line, 70Z/3. The activator LPS does not affect EP1 nor EP3beta mRNA expression. Treatment with dbcAMP, an analog of cAMP, mimics PGE-induced growth inhibition indicating that Gs-coupled EP2 and/or EP4 receptors mediate this inhibitory signal. Indeed, EP2 agonists mimic PGE2-induced growth inhibition unlike IP, EP1 and EP3-selective agonists. These data indicate that EP2 receptors are sufficient for mediating PGE-induced growth inhibition of susceptible B lineage cells.
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PMID:A molecular analysis of PGE receptor (EP) expression on normal and transformed B lymphocytes: coexpression of EP1, EP2, EP3beta and EP4. 860 22

Pulmonary parenchymal involvement in SSc is characterized by alveolitis and interstitial fibrosis, with an increased number of CD8+ T cells in BAL fluids. This study analyzed the diversity of the alphabeta T-cell repertoire in peripheral blood and BAL fluids from seven SSc patients, looking for evidence of antigen-driven selection of T cells in the lungs. A reverse transcriptase-polymerase chain reaction technique was used to amplify rearranged TCR transcripts from unfractionated, CD4+, and CD8+ T cells. Nearly all AV and BV gene families were expressed in SSc patients and most had similar levels of expression in blood and BAL samples. Next, the diversity of TCR junctional region lengths was assessed, using sequencing gel electrophoresis. Many V gene families had a Gaussian distribution of their junctional region lengths. However, some V gene families had an abnormal pattern of junctional lengths, with skewing away from a Gaussian distribution, including predominance of one or two lengths. This suggests selected expansion of T cells expressing those V genes. Alterations in TCR junctional region lengths were most prominent in bronchoalveolar CD8+ T cells, with similar patterns of skewing in several patients and in one patient over time. Sequence analysis of AV14 and BV17 junctional regions confirmed the oligoclonal character of expansion of bronchoalveolar CD8+ T cells.
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PMID:Skewing of the CD8+ T-cell repertoire in the lungs of patients with systemic sclerosis. 882 77

Surfactant protein D (SP-D) appears to play an important role in regulating local pulmonary inflammatory responses to pathogens. There is also in vitro evidence that SP-D may suppress local T cell responses. However, the role of SP-D in regulating T cell responses directly in the lung has not been previously evaluated in vivo. SP-D(-)(/-) mice demonstrate peribronchial and perivascular accumulations of lymphocytes. Therefore, we investigated the functional status and abundance of intrapulmonary lymphocytes in SP-D(-)(/-) mice. By morphometric analysis, SP-D(-)(/-) mice demonstrated increased numbers of airway- and vessel-associated lymphocytes without increases in interstitial lymphocytes. There was increased proliferative activity of lymphocytes isolated by enzymatic disassociation of minced lung. Flow cytometry was used to determine the number and functional activation status of intrapulmonary CD4(+) and CD8(+) T cells, as well as B cells and NK cells. Cytokine expression patterns in lung tissues were evaluated using RNase protection assays, reverse transcriptase/polymerase chain reaction, and enzyme-linked immunosorbent assay. There was marked T cell activation in the lungs of SP-D(-)(/-) mice, as reflected by an increased percentage of both CD4(+) and CD8(+) T cells expressing CD69 and CD25. BAL CD4 lymphocytes were increased and the fraction expressing CD69 was also increased. Although there were increases in BAL CD8 lymphocytes, apparent increases in CD69-positive CD8 lymphocytes did not reach statistical significance. In contrast, splenic T cells were not activated in SPD(-)(/-) mice. Of the proinflammatory cytokines evaluated, only interleukin (IL)-12 and IL-6 expression were consistently upregulated in the lungs of SPD(-)(/-) mice. Increased IL-2 expression was apparent but did not reach statistical significance. We conclude that the lack of local pulmonary production of SP-D leads to a state of persistent T cell activation, possibly in response to exogenous antigens. This study therefore provides further evidence of the important local immunoregulatory role of SP-D in vivo.
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PMID:Lymphocyte activation in the lungs of SP-D null mice. 1209 Dec 42

In this retrospective study, matched peripheral blood and lung samples from patients on antiretroviral therapy were studied in order to investigate whether differences in mutations associated with resistance to nucleoside analogues could be detected between the lung and blood. Discordant mutation patterns in the reverse transcriptase (RT) between plasma and cell free bronchoalveolar lavage fluid (BAL-fluid) HIV-1 genomic RNA was observed in five out of seven patients on nucleoside reverse transcriptase inhibitor (NRTI) monotherapy and six out of seven on combination therapy. In the cellular compartments, DNA recovered from peripheral blood mononuclear cells (PBMCs) and cells from BAL-cells discordant HIV-1 resistance genotypes were detected in 15 out of 44 matched samples. Differences in resistant genotypes between PBMCs and BAL-cells were most pronounced in patients receiving combination antiretroviral therapy. The pattern and number of mutations in RT associated with resistance differed in the BAL-cells compared to PBMCs in four out of 12 subjects not receiving antiretroviral therapy at the time of bronchoscopy, three from 14 patients on NRTI monotherapy, five out of nine on dual combination therapy and three out of nine on HAART. The differences in the detection of resistance mutations between blood and the lung suggest that the lung is a site of replication for HIV-1.
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PMID:Different resistance mutations can be detected simultaneously in the blood and the lung of HIV-1 infected individuals on antiretroviral therapy. 1474 57