Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:6.2.1.7 (BAL)
 1,977 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The relationship between signals generated via the sIgR complex of B lymphocytes and subsequent changes in gene expression is poorly understood at the molecular level. To illuminate mechanisms that may couple these events, we examined the expression and function of tetradecanoyl phorbol acetate-response element (TRE)-binding proteins (i.e., activator protein 1, (AP-1)) in the murine B lymphoma cell line BAL-17.7.1 (BAL-17), which models primary B lymphocyte responses in a number of respects. Cross-linking of sIgR led to substantial induction of nuclear AP-1, in BAL-17 B cells, that bound the TRE, as detected by electrophoretic mobility shift assay. The sIgR-induced TRE-binding activity consisted of both Jun and Fos proteins, on the basis of immunoreactivity of nucleoprotein complexes with specific antisera. In addition, immunoprecipitation with specific antisera showed that de novo synthesis of Jun-B and c-Jun proteins, accompanied by c-Fos, was stimulated after cross-linking of sIgR on BAL-17 B cells. Transient transfection of BAL-17 B cells with reporter gene constructs showed that B cell AP-1 failed to trans-activate the TRE-containing human collagenase gene promoter, for which activity is dependent upon functional expression of cellular c-Jun. In contrast, sIg-induced AP-1 trans-activated a HSV-tk promoter that contained three TRE; this pattern of gene expression is consistent with the presence of functional Jun-B-containing AP-1 in B lymphocytes. These results are the first to attribute a functional role to sIgR-mediated AP-1 in B lymphoid cells and suggest that AP-1 functions to couple the sIgR complex to changes in nuclear gene expression.
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PMID:Surface Ig receptor-induced nuclear AP-1-dependent gene expression in B lymphocytes. 163 70

Collagenase, collagenolytic activity and tissue inhibitor of metalloproteinases were evaluated in bronchoalveolar lavage from 25 patients with hypersensitivity pneumonitis and four control subjects. Patients were followed between two and three years, after which they were classified as "healed," "improved," or "worsened." In control samples, immunoreactive collagenase was not detected. The enzyme was present in four of seven patients who healed, six of ten patients who improved, and four of eight patients who worsened. There was no relationship between the presence or absence of BAL collagenase or its concentration and the evolution of the disease. Latent collagenolytic activity was detected only in 5 of the 14 patients who displayed immunoreactive collagenase. Regarding collagenase inhibitor, TIMP was present in BAL fluid from all patients and normal subjects. Although the highest values were found in two cases who healed or improved, there was not a statistically significant difference among the three groups of patients, neither between patients nor control subjects. These findings suggest that at least in HP, the presence of collagenase, collagenolytic activity, or TIMP in BAL fluid is not associated with the prognosis of the disease.
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PMID:Collagenase and collagenase inhibitors in bronchoalveolar lavage fluids. 164 37

Collagenases in bronchoalveolar lavage fluid (BALF) of patients with bronchiectasis and healthy subjects were characterized using specific functional and immunologic assays. The BAL fluid contained interstitial collagenase and collagenolytic proteinases of bacterial origin. Collagenase activities, obtained after organomercurial activation, correlated with the severity of bronchiectasis. In severe cases, collagenase activities were 3.5 x 10(-7) IU/L/48 h or 4.8 x 10(-6) IU/g/48 h (p < 0.01), in moderate ones 1.74 x 10(-7) IU/L/48 h or 3.35 x 10(-6) IU/g/48 h (p < 0.05), and in mild cases 0.32 x 10(-7) IU/L/48 h or 0.7 x 10(-6) IU/g/48 h (p < 0.05). The corresponding activities in healthy control subjects were 0.08 x 10(-7) IU/L/48 h or 0.13 x 10(-6) IU/g/48 h. The cellular origin of interstitial collagenase was assessed with doxycycline inhibition test utilizing the differential sensitivity of fibroblast-type collagenase/MMP-1 (IC50 = 280 microM) and neutrophil-type collagenase/MMP-8 (IC50 = 26 microM) to the anticollagenolytic, nonantimicrobial doxycycline action. Interstitial collagenase, contained in BALF, was totally inhibited by 100 microM of doxycycline. It can therefore be concluded that most of mammalian collagenase presented in inflamed fluid of bronchiectasis originated from neutrophils. The molecular forms of neutrophil-type collagenase/MMP-8 were confirmed and analyzed by Western-blot, which showed evidence of the proteolytic conversion of the latent 85-kD MMP-8 proenzyme species into active 65-kD molecular weight species. These findings strongly suggest involvement of proteolytic activation pathway of proMMP-8, especially in severe and moderate forms of bronchiectasis. Furthermore, collagenolytic proteases of bacterial origins may also participate in tissue destruction of the lung.
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PMID:Human neutrophil collagenase (MMP-8), identified in bronchiectasis BAL fluid, correlates with severity of disease. 778 60

Short-term exposure of rats to ozone results in lung inflammation characterized by increased permeability damage and the infiltration of neutrophils into the airways. The present study compared these ozone-induced inflammatory responses in different strains of male rat, Brown Norway rats from Charles River Laboratories, Inc. (BN-CRL), and Harlan Sprague Dawley, Inc. (BN-HSD), and Fischer 344 (F344), Sprague-Dawley (SPD), and Wistar (WSTR) male rats from Hilltop Lab Animals, Inc. Ozone-induced permeability damage was indicated by recoveries of bronchoalveolar lavage fluid (BALF) albumin 20 h following single exposures of 6 h to either air or 1 ppm or 2 ppm O3. Although BALF albumin recoveries from air-exposed rats were not significantly different between strains, ozone exposures resulted in a range of enhancements of BALF albumin of 2-, 9-, 17-, 7-, and 20-fold following exposures of BN-CRL, BN-HSD, F344, SPD, and WSTR rats to 2 ppm ozone, respectively. Concomitant strain differences in the number of ozone-induced BAL-recoverable neutrophils were not observed, except for BN-CRL rats, which demonstrated significantly lower numbers. However, the degree of ozone-induced permeability damage did directly correspond to differences observed in the numbers of neutrophils and eosinophils in the peripheral blood and collagenase tissue digest of lavaged and perfused lungs prior to ozone exposure. Ozone-resistant BN-CRL rats exhibited the highest numbers of blood and lung tissue neutrophils and eosinophils when compared with ozone-susceptible WSTR rats exhibiting the lowest number of these granulocytes. These data suggested that the presence of high numbers of blood and tissue granulocytes at the onset of short-term ozone exposures might provide a certain degree of protection against subsequent pathological events.
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PMID:Lung tissue neutrophil content as a determinant of ozone-induced injury. 1098 20

Forty five smokers were classified into schistosomal cases with type-2 diabetis mellitus (GI) and with associated history of bronchial asthma (GII) and without T-2 DM (GIII). A control group (GIV) of non-diabetic non schistosomal age matched subjects who quitted smoking for >6 months were included. Assessed parameters included indices of glycemic status (glycated hemoglobin), angiogenesis (vascular endothelial growth factor) hepatic and bronchoalveolar disposition (Liver function test, metallothionein, serum levels of cotinine, cadmium selenium, copper & zinc) and bronchoalveolar lavage) (BAL) levels of surfactant proteins A & D, zinc and copper oxidative stress and fibrogenesis (total antioxidant capacity thiobarbituric acid reactive substance) and vasculopathy (angiotensin converting enzyme, P-selectin, nitrate) and periodontitis (collagenase and elastase in GCF) impact of cigarette smoking associated with trace element disbalance and enzymatic changes in crevicular fluid on altered parameters collaborative out-come. The study reflected the collaborative outcome of immune mediated mechanisms initiated by liver affection, glycemic status and history of predisposed bronchial integrity induced by oxidative stress.
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PMID:Cigarette smoking induced liver insult concomitant with inflammatory mediators in serum crevicular fluid and bronchio alveolar lavage of schistosomal diabetic subjects with history of bronchial asthma. 1792 10