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:3.4.21.4 (trypsin)
42,187 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

E, EA and EAC rosetting techniques and Ig fluorescence were used in a study of receptor sites in cryostat sections of lesions through the spectrum of leprosy, and for comparison in some other mycobacterial and granulomatous lesions. Anti-C3, and trypsin were used as blocking agents. Lymphocytes in borderline lepromatous leprosy produced EA adherence and IgG fluorescence indicating B type cells. Lymphocytes in tuberculoid leprosy produced neither E or EA adherence and no fluorescence; these cells were presumed to be T cells. EAC and EA adherence was more marked in areas of macrophage infiltration, where there were few lymphocytes, than over the lympocytes themselves. Two distinct patterns emerged: (i) EA binding together with IgG fluorescence was seen in active lepromatous leprosy and could be localised to the surface of individual macrophages, and (ii) EAC binding together with IgM fluorescence was seen in the granuloma of tuberculoid leprosy and sarcoidosis, but could not be definitely related to cell surface; rather it was diffusely spread over the whole granuloma; EAC adherence was diminished by anti-C3 serum. Trypsin removed EA binding completely, but only diminished EAC adherence. It is suggested that the EA pattern indicates immunoglobulin receptors on macrophage and lymphocyte surfaces: and that the EAC binding (which is stronger than EA) involves C3 and IgM receptors at extracellular sites as well as C3 receptor sites on epithelioid cell surfaces. EA and EAC binding were enhanced in borderline tuberculoid leprosy in reaction and erythema nodosum leprosum, suggesting that immunoglobulin and complement receptor sites increase in number with enhanced hypersensitivity.
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PMID:Surface markers on lymphocytes and cells of the mononuclear phagocyte series in skin sections in leprosy. 72 93

1. Mast cell activation in the lung was investigated by measuring concentrations of mast cell tryptase and histamine in the bronchoalveolar lavage fluid from patients with bronchial carcinoma, sarcoidosis, extrinsic allergic alveolitis or cryptogenic fibrosing alveolitis and from normal subjects. 2. Histamine concentrations in bronchoalveolar lavage fluid supernatants were elevated in the bronchial carcinoma and cryptogenic fibrosing alveolitis groups, and were correlated with the histamine content of the cells recovered. 3. An avidin-biotin-enhanced antigen-capture e.l.i.s.a., using polyclonal rabbit antibody specific for tryptase, and mouse monoclonal antibody AA5, allowed the quantification of tryptase in all samples of bronchoalveolar lavage fluid. Tryptase concentrations were increased in the bronchial carcinoma and extrinsic allergic alveolitis groups and in some of the patients with sarcoidosis, and the levels correlated with mast cell numbers and also with concentrations of albumin. 4. There was no significant correlation between levels of tryptase and histamine, suggesting differences in the rates of metabolism or different cellular sources. 5. The tryptase and histamine concentrations measured suggest that there is continuous degranulation of mast cells within the normal lung, but that this process is more pronounced in patients with bronchial carcinoma or interstitial lung disease.
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PMID:Mast cell tryptase and histamine concentrations in bronchoalveolar lavage fluid from patients with interstitial lung disease. 165 61

In patients with pulmonary diseases, serum alpha 1-antitrypsin (AAT) was measured by three methods: radial immunodiffusion (RID), trypsin inhibitory capacity assay (TIC) and by rate nephelometry with the immunosystem (NIA) in a total of 369 subjects (sarcoidosis, n = 35; asthma, n = 41; chronic obstructive bronchitis, n = 62; bronchogenic carcinoma, n = 93; pneumonia, n = 24; tuberculosis, n = 43; fibrosis, n = 22; healthy controls, n = 49). Considering all patients, AAT was found to be significantly elevated (p less than 0.01-0.001) in all methods (RID: 3.3 +/- 1.0 g/l; TIC: 2.7 +/- 0.4 g/l; NIA: 2.1 +/- 0.8 g/l) compared to healthy controls (RID: 2.1 +/- 0.3 g/l; TIC: 2.1 +/- 0.4 g/l; NIA: 1.2 +/- 0.3 g/l). The lowest mean values were found by means of the NIA method. The best correlation coefficient (R) was evaluated between the TIC and the NIA method (R = 0.96) in healthy controls, but the best correlated methods were the RID and the NIA (R = 0.93) in patients with pulmonary disease.
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PMID:Comparison of three methods for the determination of serum alpha-1-antitrypsin in patients with pulmonary diseases. 250 24

Human alveolar macrophages (AM) obtained by bronchoalveolar lavage (BAL) were found to bear cytophilic IgA and Fc alpha-receptors (Fc alpha R) on their surface. The cytophilic IgA belongs to the IgA1 subclass, but unoccupied receptors can be saturated with either IgA1 or IgA2 molecules. Although both polymeric and monomeric forms could attach, binding was about 5-fold greater for the polymers. Both cytophilic IgA and Fc alpha R are sensitive to trypsin and disappear after 18 h of AM culture. An increase in cytophilic IgA was observed on AM from untreated patients with pulmonary sarcoidosis, but not on AM from steroid-treated patients. A significant correlation was found between IgA levels in BAL and the percentage of AM with cytophilic IgA in normal subjects and in steroid-treated sarcoid patients. However, no such relationship was seen among untreated patients. These data suggest that multiple factors may modulate AM surface receptors for IgA. Inflammatory events occurring in the lungs could alter receptor expression and perhaps be of significance in the immunophysiopathology of certain pulmonary diseases.
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PMID:Surface IgA and Fc-alpha receptors on human alveolar macrophages from normal subjects and from patients with sarcoidosis. 292 74

The status of the blood kinin system, activity of serum inhibitors of proteinases (alpha 1-protease inhibitor and alpha 2-macroglobulin) as well as indices of activity of trypsin-like proteinases, elastolytic and fibrinolytic activity, free antitryptic activity and complete content of acid stable inhibitors were studied in the morning sputum and bronchoalveolar washesoff of 62 patients with intrathoracic sarcoidosis. It was shown that in active sarcoidosis proteinase-inhibitors balance got disturbed as a result of a decrease in the activity of serum inhibitors, suppression of local secretion of acid stable inhibitors and inactivation at the level of alpha 1-protease inhibitor alveoles. Excessive activation of the kinin system was noted in the blood flow and elevation of all types of proteolytic activity in the respiratory system. It was assumed that the above changes reflected disturbed self-control processes in the body and caused progression of disease and pneumofibrosis formation.
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PMID:[The kallikrein-kinin system of the blood and protease-protease inhibitor balance in active sarcoidosis]. 325 20

Anterior uveitis or iritis occurs in a variety of systemic diseases including sarcoid, Behcet's, and spondyloarthritis. Iritis is, therefore, presumed to result from a variety of pathogenetic mechanisms. We hypothesized that unique chemotactic factors should be associated with different etiologies for inflammation. We have tested this hypothesis using rabbit models of anterior uveitis. We have found that aqueous humor generally contained chemotactic activity for monocytes 24 h after an intravitreal injection of endotoxin, killed mycobacteria, or human serum albumin (in a rabbit previously immunized against human serum albumin). Anterior chamber paracentesis resulted in aqueous humor with a high protein content. However, in contrast to the other models of inflammation, paracentesis did not result in a cellular infiltrate in the anterior chamber, and aqueous humor after paracentesis was not chemotactic. For either immunologically mediated inflammation or for inflammation resulting from injection of a killed bacterial product, chemotactic activity could be digested by papain or trypsin and tended to coelute with albumin on either gel filtration or ion-exchange chromatography. These observations suggest that a similar chemotactic factor for monocytes appears to be associated with ocular inflammation that follows either an immune response or injection of a killed bacterial product.
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PMID:Similar chemotactic factor for monocytes predominates in different animal models of uveitis. 341 43

Sarcoid macrophage-epithelioid cells have been shown to release a growth factor that stimulates the proliferation of vascular endothelial cells in vitro. In the presence of this factor, cultured endothelial cells can proliferate in a serum-free medium. Gel-chromatography on Sephadex G-75 revealed a single peak of activity on endothelial cells. The molecular weight was estimated at 7,000-10,000. The activity was heat-labile and trypsin-sensitive, and did not adhere to heparin-Sepharose.
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PMID:A macrophage factor that stimulates the proliferation of vascular endothelial cells. 394 29

Circulating immune complexes were present in half of 31 patients with sarcoidosis and raised levels were associated with low numbers of T suppressor cells (T gamma- and Fc gamma-receptor-positive lymphocytes). Incubation of T cells with trypsin restored the percentage of T gamma cells to within or above the normal range. Incubation of normal lymphocytes with sarcoid immune complexes significantly reduced the number of detectable T gamma cells. Preincubation of normal lymphocytes with circulating immune complexes significantly reduced their blastogenic response to concanavalin A. These studies suggest an interaction between immune complexes and T suppressor cells in sarcoidosis and emphasise the importance of immune complexes in modulating the immune response.
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PMID:Interaction of immune complexes and T suppressor cells in sarcoidosis. 621 75

Angiotensin I converting enzyme (kininase II, peptidyl dipeptidase, ACE) was purified by reverse immunoadsorption from a membrane fraction of the human kidney. ACE is very likely a transmembrane peptidase. Treatment of the membrane-bound enzyme with trypsin releases a low mol. wt. fragment (greater than 10,000), which is probably the anchor peptide inserted into the plasma membrane. Antibody to ACE was used to localize it in the CNS where it is bound to plasma membrane of neuroepithelial cells in structures such as the globus pallidus or substantia nigra. Radioimmunoassay indicated that ACEs of endothelial, epithelial and neuroepithelial origin are immunologically identical. Direct radioimmunoassay also showed that there is a strong negative correlation between plasma enzyme level and pulmonary diffusing capacity of sarcoid patients. Finally, in addition to various peptides, homogeneous human ACE cleaves fluorogenic substrates where the C-terminal amino acid is replaced with nitrobenzylamine.
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PMID:Human converting enzyme. 631 67

An increased (p < 0.001) frequency of bronchial hyperreactivity (BHR) was found in sarcoidosis patients as compared with healthy volunteers. The patients had more mast cells (p < 0.001) and tryptase (p < 0.001) in their bronchoalveolar lavage fluid, but there were no differences between BHR-positive and BHR-negative patients. Furthermore, the bronchoalveolar lavage fluid concentrations of macrophages, lymphocytes, and of the soluble components albumin, fibronectin, and vitronectin were also elevated in the sarcoidosis patients, indicating an ongoing inflammation in the airways and/or in the interstitium. We observed no significant differences in the parameters when the sarcoidosis patients were subdivided into BHR, clinical activity, or chest X-ray stages. Our findings may indicate a multifactorial background to the hyperreactivity.
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PMID:Sarcoidosis patients have bronchial hyperreactivity and signs of mast cell activation in their bronchoalveolar lavage. 756 33


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