Imperial College London

Professor Terry Tetley

Faculty of MedicineNational Heart & Lung Institute

Professor of Lung Cell Biology
 
 
 
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Contact

 

+44 (0)20 7594 2984t.tetley Website

 
 
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Location

 

109Sir Alexander Fleming BuildingSouth Kensington Campus

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Summary

 

Publications

Publication Type
Year
to

212 results found

MISTRY R, SNASHALL PD, TOTTY N, GUZ A, TETLEY TDet al., 1991, ISOLATION AND CHARACTERIZATION OF SHEEP ALPHA-1-PROTEINASE INHIBITOR, BIOCHEMICAL JOURNAL, Vol: 273, Pages: 685-690, ISSN: 0264-6021

Journal article

PAI V, GUZ A, PHILLIPS GJ, COOKE NT, HUTCHISON DCS, TETLEY TDet al., 1991, URINARY DESMOSINE, ELASTOLYSIS, AND LUNG-DISEASE, METABOLISM-CLINICAL AND EXPERIMENTAL, Vol: 40, Pages: 139-145, ISSN: 0026-0495

Journal article

SMITH SF, GOULDING NJ, GODOLPHIN JL, TETLEY TD, ROBERTS CM, GUZ A, FLOWER RJet al., 1990, AN ASSAY FOR THE ASSESSMENT OF LIPOCORTIN-1 LEVELS IN HUMAN LUNG LAVAGE FLUID, JOURNAL OF IMMUNOLOGICAL METHODS, Vol: 131, Pages: 119-125, ISSN: 0022-1759

Journal article

Bingle L, Bull TB, Fox B, Guz A, Richards RJ, Tetley TDet al., 1990, Type II pneumocytes in mixed cell culture of human lung: a light and electron microscopic study, Environmental Health Perspectives, Vol: 85, Pages: 71-80, ISSN: 1552-9924

Journal article

Smith SF, Tetley TD, Guz A, Flower RJet al., 1990, Detection of lipocortin 1 in human lung lavage fluid: lipocortin degradation as a possible proteolytic mechanism in the control of inflammatory mediators and inflammation, Environmental Health Perspectives, Vol: 85, Pages: 135-144, ISSN: 1552-9924

Journal article

TETLEY TD, SMITH SF, WINNING AJ, FOXALL JM, COOKE NT, BURTON GH, HARRIS E, GUZ Aet al., 1989, THE ACUTE EFFECT OF CIGARETTE-SMOKING ON THE NEUTROPHIL ELASTASE INHIBITORY CAPACITY OF PERIPHERAL LUNG LAVAGE FROM ASYMPTOMATIC VOLUNTEERS, EUROPEAN RESPIRATORY JOURNAL, Vol: 2, Pages: 802-810, ISSN: 0903-1936

Journal article

Griffin NR, Wells M, Fox H, Lee YS, Raju GC, Howie AJ, Brewer DB, Wilkinson M, McCartney ACE, Fox B, Partridge TA, Macrae KD, Tetley TD, Phillips GJ, Guz Aet al., 1989, Letters to the editor, The Journal of Pathology, Vol: 157, Pages: 153-155, ISSN: 0022-3417

Journal article

SMITH SF, GUZ A, WINNING AJ, COOKE NT, BURTON GH, TETLEY TDet al., 1988, COMPARISON OF HUMAN-LUNG SURFACE PROTEIN PROFILES FROM THE CENTRAL AND PERIPHERAL AIRWAYS SAMPLED USING 2 REGIONAL LAVAGE TECHNIQUES, EUROPEAN RESPIRATORY JOURNAL, Vol: 1, Pages: 792-800, ISSN: 0903-1936

Journal article

MCCARTNEY ACE, FOX B, PARTRIDGE TA, MACRAE KD, TETLEY TD, PHILLIPS GJ, GUZ Aet al., 1988, EMPHYSEMA IN THE BLOTCHY MOUSE - A MORPHOMETRIC STUDY, JOURNAL OF PATHOLOGY, Vol: 156, Pages: 77-81, ISSN: 0022-3417

Journal article

FOX B, BULL TB, GUZ A, HARRIS E, TETLEY TDet al., 1988, IS NEUTROPHIL ELASTASE ASSOCIATED WITH ELASTIC TISSUE IN EMPHYSEMA, JOURNAL OF CLINICAL PATHOLOGY, Vol: 41, Pages: 435-440, ISSN: 0021-9746

Journal article

Smith SF, Guz A, Burton GH, Heaton R, Cooke NT, Tetley TDet al., 1988, The elastase: anti-elastase profile in lung lavage from sarcoidosis patients., Sarcoidosis, Vol: 5, Pages: 31-37, ISSN: 0393-1447

One feature of pulmonary sarcoidosis is an increase of lymphocyte numbers in bronchoalveolar lavage fluid (BALF). In some patients the number of polymorphonuclear neutrophils (PMN) also rises. It has been suggested that the prognosis for the latter subjects is likely to be worse than that for the former, but the damaging agent (or agents) released by the PMN have not yet been identified. Therefore, in the current study, the activity of one neutrophilic enzyme, elastase, which is known to damage the pulmonary interstitium, has been assessed in sarcoid BALF and compared to BALF from subjects matched for age, sex and smoking status. As BALF also contains locally-produced and serum-derived inhibitors of elastase, levels of which may change in subjects with sarcoidosis, the serine protease inhibitory capacity and the levels of three anti-elastases have been measured in the samples. Levels of the serum-derived antiproteases, alpha 1 proteinase inhibitor (alpha 1PI) and alpha 2 macroglobulin (alpha 2M) were found to be significantly increased. However, alpha 1PI/albumin and alpha 2M/albumin ratios were unchanged, suggesting that the increased levels were due to an increased permeability of the alveolar-capillary barrier. The total protease inhibitory capacity was elevated and this could be entirely explained by the raised levels of alpha 1PI and alpha 2M. Levels of the locally-produced inhibitor were unaltered. The elastolytic capacity of sarcoid BALF was unchanged. Thus, the elastase: anti-elastase balance was shifted against elastolytic activity.(ABSTRACT TRUNCATED AT 250 WORDS)

Journal article

SMITH SF, GUZ A, BURTON GH, COOKE NT, TETLEY TDet al., 1988, COMPARISON OF ELASTOLYTIC ACTIVITY IN LUNG LAVAGE FROM CURRENT, EX-SMOKERS AND NON-SMOKERS, LIFE SCIENCES, Vol: 43, Pages: 459-464, ISSN: 0024-3205

Journal article

Tetley TD, Smith SF, Burton GH, Winning AJ, Cooke NT, Guz Aet al., 1987, Effects of cigarette smoking and drugs on respiratory tract proteases and antiproteases., Eur J Respir Dis Suppl, Vol: 153, Pages: 93-102, ISSN: 0106-4347

Increased pulmonary proteolytic (elastolytic) activity is thought to be the primary cause of emphysema and may also play a rôle in the pathology of bronchitis. These diseases are common amongst tobacco smokers. Serum-derived alpha 1-proteinase inhibitor (alpha 1PI) and locally produced protease inhibitors normally protect the pulmonary epithelium from proteolytic attack, but tobacco smoke can inactivate these antiproteases by oxidative and non-oxidative mechanisms. Bronchoalveolar lavage fluid (BALF) samples lung surface components and most studies show that there is elevated elastolytic activity in smokers' BALF. Whether antiproteolytic capacity is reduced in these samples remains debatable. A selective lavage technique is described which independently samples central and peripheral epithelium from the same subject. Analysis demonstrates a protease-antiprotease imbalance which can differ in central and peripheral lavage and which could be significant in the development of obstructive airways disease. Therapeutic approaches include augmenting antiprotease potential using genetically engineered, oxidant-resistant alpha 1PI or synthetic peptide inhibitors.

Journal article

SMITH SF, GUZ A, BURTON GH, COOKE NT, TETLEY TDet al., 1986, ACID-STABLE LOW-MOLECULAR MASS PROTEINASE-INHIBITORS IN HUMAN-LUNG LAVAGE, BIOLOGICAL CHEMISTRY HOPPE-SEYLER, Vol: 367, Pages: 183-189, ISSN: 0177-3593

Journal article

Smith SF, Guz A, Cooke NT, Winning AJ, Foxall J, Tetley TDet al., 1986, Effects of cigarette smoke on antiproteases at the human lung surface., Eur J Respir Dis Suppl, Vol: 146, Pages: 139-143, ISSN: 0106-4347

Journal article

SMITH SF, GUZ A, COOKE NT, BURTON GH, TETLEY TDet al., 1985, EXTRACELLULAR ELASTOLYTIC ACTIVITY IN HUMAN-LUNG LAVAGE - A COMPARATIVE-STUDY BETWEEN SMOKERS AND NON-SMOKERS, CLINICAL SCIENCE, Vol: 69, Pages: 17-27, ISSN: 0143-5221

Journal article

STOCKLEY RA, MORRISON HM, SMITH S, TETLEY Tet al., 1984, THE QUANTITATION AND FUNCTION OF PROTEINASE-INHIBITORS IN SPUTUM AND BRONCHOALVEOLAR LAVAGE, Publisher: BRITISH MED JOURNAL PUBL GROUP, Pages: 238-238, ISSN: 0040-6376

Conference paper

LAURENT GJ, TETLEY TD, 1984, PULMONARY FIBROSIS AND EMPHYSEMA - CONNECTIVE-TISSUE DISORDERS OF THE LUNG, EUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Vol: 14, Pages: 411-413, ISSN: 0014-2972

Journal article

STOCKLEY RA, MORRISON HM, SMITH S, TETLEY Tet al., 1984, LOW-MOLECULAR MASS BRONCHIAL PROTEINASE-INHIBITOR AND ALPHA-1-PROTEINASE INHIBITOR IN SPUTUM AND BRONCHOALVEOLAR LAVAGE, HOPPE-SEYLERS ZEITSCHRIFT FUR PHYSIOLOGISCHE CHEMIE, Vol: 365, Pages: 587-595, ISSN: 0018-4888

Journal article

WHITE LR, HUNT J, TETLEY TD, RICHARDS RJet al., 1981, BIOCHEMICAL AND CELLULAR EFFECTS OF WELDING FUME PARTICLES IN THE RAT LUNG, ANNALS OF OCCUPATIONAL HYGIENE, Vol: 24, Pages: 93-101, ISSN: 0003-4878

Journal article

RICHARDS RJ, ROSE FA, TETLEY TD, COBB LM, HARDY CJet al., 1981, EFFECTS IN THE RAT OF INHALING PVC DUST AT THE NUISANCE DUST LEVEL (10 MG-M3), ARCHIVES OF ENVIRONMENTAL HEALTH, Vol: 36, Pages: 14-19, ISSN: 0003-9896

Journal article

TETLEY TD, ROSE FA, RICHARDS RJ, 1981, BIOCHEMICAL AND CELLULAR REACTION OF PVC PASTE POLYMERS AND LATEX FOLLOWING INTRA-TRACHEAL INSTILLATION INTO RATS, INFLAMMATION, Vol: 5, Pages: 137-152, ISSN: 0360-3997

Journal article

RICHARDS RJ, TETLEY TD, HUNT J, 1981, THE BIOLOGICAL REACTIVITY OF CALCIUM SILICATE COMPOSITES - INVIVO STUDIES, ENVIRONMENTAL RESEARCH, Vol: 26, Pages: 243-257, ISSN: 0013-9351

Journal article

Desai R, Tetley TD, Curtis CG, Powell GM, Richards RJet al., 1978, Studies on the fate of pulmonary surfactant in the lung., Biochem J, Vol: 176, Pages: 455-462, ISSN: 0264-6021

1. Radioactively labelled pulmonary surfactant was prepared in an isolated perfused lung system provided with [14C]hexadecanoate. 2. After intratracheal administration of pulmonary surfactant radioactively labelled components were rapidly distributed into different lung fractions, including macrophages (free cells), but most of the radioactive label was accumulated by the lung tissue. 3. Alveolar macrophages, maintained in a variety of culture media in the presence and absence of mineral particles, incorporated a low percentage (11%) of radioactively labelled components when incubated with the surfactant, although evolution of labelled CO2 (6% of the original total activity) suggested that some breakdown of the components had taken place. 4. In similar cultures little intracellular accumulation or extracellular release of non-esterified fatty acids was demonstrated, indicating minimal catabolism of the high-molecular-weight lipid components of surfactant (particularly phosphatidylcholine). 5. However, experiments in vitro designed to simulate the lysosomal degradation of endocytosed surfactant indicated that the macrophage had enzymes capable of releasing non-esterified fatty acids, particularly hexadecanoate, from the lipoprotein complex. 6. It is argued that lung cells, other than alveolar macrophages, may also have a role in surfactant turnover.

Journal article

DESAI R, TETLEY TD, CURTIS CG, POWELL GM, RICHARDS RJet al., 1978, STUDIES ON FATE OF PULMONARY SURFACTANT IN LUNG, BIOCHEMICAL JOURNAL, Vol: 176, Pages: 455-462, ISSN: 0264-6021

Journal article

TETLEY TD, RICHARDS RJ, HARWOOD JL, 1977, CHANGES IN PULMONARY SURFACTANT AND PHOSPHATIDYLCHOLINE METABOLISM IN RATS EXPOSED TO CHRYSOTILE ASBESTOS DUST, BIOCHEMICAL JOURNAL, Vol: 166, Pages: 323-329, ISSN: 0264-6021

Journal article

TETLEY TD, DESAI R, HARWOOD JL, POWELL GM, CURTIS CG, RICHARDS RJet al., 1977, UTILIZATION OF (H-3)LEUCINE AND (C-14)HEXADECANOIC ACID BY ISOLATED PERFUSED RABBIT LUNG FOR BIOSYNTHESIS OF RADIOLABELED PULMONARY SURFACTANT, BIOCHEMICAL SOCIETY TRANSACTIONS, Vol: 5, Pages: 1310-1312, ISSN: 0300-5127

Journal article

Tetley TD, Desai R, Harwood JL, Powell GM, Curtis CG, Richards RJet al., 1977, The utilization of [3H] leucine and [14C] hexadecanoic acid by the isolated perfused rabbit lung for biosynthesis of radiolabelled pulmonary surfactant [proceedings]., Biochem Soc Trans, Vol: 5, Pages: 1310-1312, ISSN: 0300-5127

Journal article

TETLEY TD, HEXT PM, RICHARDS RJ, MCDERMOTT Met al., 1976, CHRYSOTILE-INDUCED ASBESTOSIS - CHANGES IN FREE-CELL POPULATION, PULMONARY SURFACTANT AND WHOLE LUNG-TISSUE OF RATS, BRITISH JOURNAL OF EXPERIMENTAL PATHOLOGY, Vol: 57, Pages: 505-514, ISSN: 0007-1021

Journal article

Richards RJ, Hext PM, Desai R, Tetley T, Hunt J, Presley R, Dodgson KSet al., 1975, Chrysotile asbestos: biological reaction potential., Inhaled Part, Vol: 4 Pt 2, Pages: 477-493, ISSN: 0301-1577

Evidence is presented indicating that chrysotile asbestos induces rapid cellular ageing in lung fibroblast cultures. Depending on the dose of asbestos given to these cultures the formation of fibrous collagen is enhanced or suppressed. The reaction of chrysotile at the cellular and molecular level is discussed and is considered to be determined by the organic coating it receives or the manner in which the surface absorbed material is modified. Studies are included of the ability of chrysotile to adsorb and retain serum proteins, pulmonary surfactant and lysosomal enzymes. Finally, a critical appraisal is given of the theories accounting for chrysotile-induced fibrogenesis particularly related to the lung fibroblast system studied.

Journal article

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