Publications
212 results found
Kemp SJ, Thorley AJ, Gorelik J, et al., 2008, Immortalization of Human Alveolar Epithelial Cells to Investigate Nanoparticle Uptake, AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY, Vol: 39, Pages: 591-597, ISSN: 1044-1549
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- Citations: 103
Valsami-Jones E, Berhanu D, Dybowska A, et al., 2008, Nanomaterial synthesis and characterization for toxicological studies:: TiO<sub>2</sub> case study, 8th International Symposium on the Geochemistry of the Earths Surface (GES-8), Publisher: MINERALOGICAL SOC, Pages: 515-519, ISSN: 0026-461X
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- Citations: 10
Thorley AJ, Tetley TD, 2007, Pulmonary epithelium, cigarette smoke, and chronic obstructive pulmonary disease, International Journal of Chronic Obstructive Pulmonary Disease, Vol: 2, Pages: 409-428, ISSN: 1176-9106
Chronic obstructive pulmonary disease (COPD) is a complex chronic inflammatory disease involving a wide variety of cells and inflammatory mediators. The most important etiological factor in the development of this disease is cigarette smoking. Much of the research into the mechanisms of COPD has been concerned with the induction of inflammation and the role of neutrophils and macrophages in the pathophysiology of the disease. The possible contribution of the epithelium to the development of COPD has only recently become apparent and remains unclear. In this article we review research into the effect of cigarette smoke on the pulmonary epithelium with particular emphasis on oxidative stress, proteolytic load, pro-inflammatory cytokine and chemokine profile and epithelial secretions. In addition, we have also reviewed how cigarette smoke may affect epithelial damage and repair processes.
Maher TM, Bottoms SE, Mercer PF, et al., 2007, Differential modulation of lung fibroblast and alveolar epithelial cell apoptosis by cyclo-oxygenase (COX)-2 and prostaglandin E<sub>2</sub> is an important mechanism in the pathogenesis of idiopathic pulmonary fibrosis, Winter Meeting of the British-Thoracic-Society, Publisher: B M J PUBLISHING GROUP, Pages: A24-A24, ISSN: 0040-6376
Tsoumakidou M, Zhu J, Wang Z, et al., 2007, Immunohistochemical detection of dendritic cells in human lung tissue, HISTOPATHOLOGY, Vol: 51, Pages: 565-568, ISSN: 0309-0167
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- Citations: 5
Tetley TD, 2007, Health effects of nanomaterials, BIOCHEMICAL SOCIETY TRANSACTIONS, Vol: 35, Pages: 527-531, ISSN: 0300-5127
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- Citations: 66
Arcaro A, Aubert M, del Hierro MEE, et al., 2007, Critical role for lipid raft-associated Src kinases in activation of PI3K-Akt signalling, CELLULAR SIGNALLING, Vol: 19, Pages: 1081-1092, ISSN: 0898-6568
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- Citations: 109
Thorley AJ, Ford PA, Giembycz MA, et al., 2007, Differential regulation of cytokine release and leukocyte migration by lipopolysaccharide-stimulated primary human lung alveolar type II epithelial cells and macrophages, JOURNAL OF IMMUNOLOGY, Vol: 178, Pages: 463-473, ISSN: 0022-1767
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- Citations: 164
Tetley TD, 2006, PROTEINASE INHIBITORS, Encyclopedia of Respiratory Medicine: Volume 1-4, ISBN: 9780123708793
Secretory leukoprotease inhibitor (SLPI) and elafin are acid-stable, low-molecular-weight antiproteinases that are produced by the goblet cells, Clara cells, and alveolar type II cells in the pulmonary epithelium, and are also present in macrophages, while neutrophils contain SLPI. SLPI inhibits neutrophil elastase, cathepsin G, trypsin, chymotrypsin, and chymase. Elafin inhibits neutrophil elastase and proteinase-3. SLPI is 11.7 kDa; elafin (6 kDa) is a cleavage product of pre-elafin (also called trappin-2), which is 9.9 kDa. The inhibitory site of both inhibitors resides in the C-terminal four disulfide whey acidic protein (WAP) domain, which has 40% homology, and they belong to the WAP family of proteins located on chromosome 20q12-13. The N-terminal WAP domain of pre-elafin contains a transglutaminase substrate domain that enables the molecule to become tethered to cell surfaces and matrix proteins; proteolytic cleavage releases the C-terminal 6 kDa inhibitory domain. SLPI is also found in close association with elastic tissue, possibly reflecting its cationic properties. SLPI and elafin have antimicrobial activity against Gram-positive and Gram-negative bacteria, while SLPI has also been shown to have antiviral and antifungal properties. In addition, SLPI and elafin are immunomodulatory, interacting directly with lipopolysaccharide to subdue its inflammatory activity, and inhibiting release of mediators from inflammatory cells. SLPI also plays a significant role in wound healing, partly by preventing proteolytic activation of proinflammatory mediators. SLPI and elafin levels and activity change during lung diseases (e.g., chronic obstructive pulmonary disease, acute respiratory distress syndrome, and pneumonia), reflecting the degree of inflammation, proteolytic load, and oxidative stress. The possibility of SLPI and elafin therapy is under active investigation.
Tetley TD, 2006, Proteinase inhibitors: Secretory Leukoprotease Inhibitor and Elafin., Encyclopedia of Respiratory Medicine, Editors: Laurent, Shapiro, Publisher: Elsevier
T D Tetley, 2005, Inflammatory cells and chronic obstructive pulmonary disease., Current Drug Targets Inflammation & Allergy, Vol: 4, Pages: 607-618, ISSN: 1568-010X
Thorley AJ, Goldstraw P, Young A, et al., 2005, Primary human alveolar type II eplithelial cell CCL20 (macrophage inflammatory protein-3α)-induced dendritic cell migration, AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY, Vol: 32, Pages: 262-267, ISSN: 1044-1549
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- Citations: 65
Tetley TD, 2005, Antiprotease therapy., Therapeutic strategies in COPD., Editors: Cazzola, Celli, Dahl, Rennard, Oxford, Publisher: Taylor & Francis, Pages: 233-246, ISBN: 9781904392422
Duggan ST, Mudway IS, Tetley T, et al., 2005, Vitamin C oxidation in human respiratory tract lining fluid cannot be solely attributed to the presence of unchelated metal ions, 13th Biennial Meeting of the Society-for-Free-Radical-Research, Publisher: TAYLOR & FRANCIS LTD, Pages: S55-S55, ISSN: 1071-5762
Pardo OE, Lesay A, Arcaro A, et al., 2004, Fibroblast growth factor 2-mediated translational control of IAPs blocks mitochondrial release of Smac/DIABLO and apoptosis in small cell lung cancer cells (vol 23, pg 7600, 2003), MOLECULAR AND CELLULAR BIOLOGY, Vol: 24, Pages: 6887-6887, ISSN: 0270-7306
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- Citations: 2
Armstrong L, Medford ARL, Uppington KM, et al., 2004, Expression of functional toll-like receptor-2 and-4 on alveolar epithelial cells, AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY, Vol: 31, Pages: 241-245, ISSN: 1044-1549
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- Citations: 181
Payne JP, Kemp SJ, Dewar A, et al., 2004, Effects of airborne World Trade Center dust on cytokine release by primary human lung cells in vitro, JOURNAL OF OCCUPATIONAL AND ENVIRONMENTAL MEDICINE, Vol: 46, Pages: 420-427, ISSN: 1076-2752
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- Citations: 36
Witherden IR, Vanden Bon EJ, Goldstraw P, et al., 2004, Primary human alveolar type II epithelial cell chemokine release - Effects of cigarette smoke and neutrophil elastase, AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY, Vol: 30, Pages: 500-509, ISSN: 1044-1549
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- Citations: 135
Maynard RM, Tetley TD, 2004, Bioterrorism: the lung under attack, THORAX, Vol: 59, Pages: 188-189, ISSN: 0040-6376
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- Citations: 3
Kendall M, Guntern J, Lockyer NP, et al., 2004, Urban PM2.5 surface chemistry and interactions with bronchoalveolar lavage fluid., Inhal Toxicol, Vol: 16 Suppl 1, Pages: 115-129, ISSN: 0895-8378
This study investigated the surface chemistry of urban fine particles (PM(2.5)), and quantified the adsorbed and desorbed species after exposure to bronchoalveolar lavage fluid (BALF). Urban background and roadside PM(2.5) samples of different mass concentration and total weight were collected in triplicate in the South Bronx region of New York City. Simultaneously, the concentrations of other atmospheric pollutants (CO, NO(x), SO(2), O(3), elemental carbon) were measured, and weather conditions were recorded. The collected PM(2.5) samples underwent one of three treatments: no treatment, treatment in vitro with BALF, or treatment in a saline solution (control). The surfaces of untreated, saline-treated, and BALF-treated PM(2.5) samples were analyzed using x-ray photoelectron spectroscopy (XPS) and time-of-flight secondary ion mass spectrometry (ToF-SIMS). These results were then compared with ambient air pollutant concentrations, weather variables, selected BALF characteristics, and results from a previous London study conducted using identical preparation methods by XPS analysis only. Both XPS and ToF-SIMS detected PM(2.5) surface species and observed changes in surface concentrations after treatment. XPS analysis showed the surface of untreated urban PM(2.5) consisted of 79 to 87% carbon and 10 to 16% oxygen with smaller contributions of N, S, Si, and P in the samples from both background and roadside locations. A wider variety of other inorganic and organic species (including metals, aliphatic and aromatic hydrocarbons, and nitrogen-containing molecules) was detected with ToF-SIMS. Surface characteristics of particles from the roadside and background sites were very similar, except for higher (p <.05) nitrate concentrations at the roadside, which were attributable to higher roadside NO(x) concentrations. Comparable species and quantities were identified in a previous study of London PM(2.5), where PM(2.5) surface chemistry differed considerably depending on th
Lucattelli M, Cavarra E, de Santi MM, et al., 2003, Collagen phagocytosis by lung alveolar macrophages in animal models of emphysema, EUROPEAN RESPIRATORY JOURNAL, Vol: 22, Pages: 728-734, ISSN: 0903-1936
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- Citations: 25
Pardo OE, Lesay A, Arcaro A, et al., 2003, Fibroblast growth factor 2-mediated translational control of IAPs blocks mitochondrial release of Smac/DIABLO and apoptosis in small cell lung cancer cells, MOLECULAR AND CELLULAR BIOLOGY, Vol: 23, Pages: 7600-7610, ISSN: 0270-7306
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- Citations: 91
Tetley TD, 2003, Smoking and the lung, Drink, Drugs and Dependence: From Science to Clinical Practice, Pages: 90-102, ISBN: 9780415278911
Payne JP, Moreno T, Richards RJ, et al., 2003, Particle-induced oxidative stress and cytokine release is attenuated by lung antioxidants in human alveolar macrophages and type 2 epithelial cells, Experimental Lung Research, Vol: 29, Pages: 421-444, ISSN: 0190-2148
Arcaro A, Khanzada UK, Vanhaesebroeck B, et al., 2002, Two distinct phosphoinositide 3-kinases mediate polypeptide growth factor-stimulated PKB activation, EMBO JOURNAL, Vol: 21, Pages: 5097-5108, ISSN: 0261-4189
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- Citations: 75
Kamal AM, Corrigan CJ, Tetley TD, et al., 2002, Effect of fluticasone on the elastase:antielastase profile of the normal lung, EUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Vol: 32, Pages: 713-719, ISSN: 0014-2972
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- Citations: 2
Tetley TD, 2002, Macrophages and the pathogenesis of COPD, CHEST, Vol: 121, Pages: 156S-159S, ISSN: 0012-3692
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- Citations: 149
Kendall M, Tetley TD, Wigzell E, et al., 2002, Lung lining liquid modifies PM<inf>2.5</inf> in favor of particle aggregation: A protective mechanism, American Journal of Physiology - Lung Cellular and Molecular Physiology, Vol: 282, ISSN: 1040-0605
The health effects of particle inhalation including urban air pollution and tobacco smoke comprise a significant public health concern worldwide, although the mechanisms by which inhaled particles cause premature deaths remain undetermined. In this study, we assessed the physicochemical interactions of fine airborne particles (PM2.5) and lung lining liquid using scanning electron microscopy, atomic force microscopy, and X-ray photon spectroscopy. We provide experimental evidence to show that lung lining liquid modifies the chemistry and attractive forces at the surface of PM2.5, which leads to enhanced particle aggregation. We propose that this is an important protective mechanism that aids particle clearance in the lung.
Tetley TD, 2002, Macrophages and the pathogenesis of COPD, Pages: 156S-159S, ISSN: 0012-3692
Macrophages are long-lived effector cells within the lung. They are reactive, responding to endogenous and exogenous stimuli, as well as proactive, producing mediators that modulate the behavior of surrounding cells. In addition, they play a critical role in the clearance of apoptotic neutrophils. Their role in COPD probably reflects a number of functional properties. However, if the link between increased proteinase burden and tissue destruction and injury in patients with COPD is correct, then macrophages must be very significant. Even though other cells, including epithelial cells and fibroblasts, have been shown to express higher matrix metalloproteinase (MMP) levels in lung tissue from subjects with COPD and emphysema, the numbers of resident cells do not appear to increase by the same factor as that of sequestered macrophages. The combination of a 5-to 10-fold increase in macrophage numbers, the up-regulation of MMPs, and their corelease with other classes of stored proteinases must be highly significant in terms of an increase in proteinase potential in the small airways and respiratory units. This may account for increased tissue destruction and inflammatory mediator activation leading to the pathology that occurs during COPD. Since only about 15% of smokers develop clinically significant disease, it seems likely, in smokers without COPD, that these processes either are strictly controlled or that lung repair mechanisms are more effective.
Kendall M, Tetley TD, Wigzell E, et al., 2002, Lung lining liquid modifies PM<sub>2.5</sub> in favor of particle aggregation:: a protective mechanism, AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY, Vol: 282, Pages: L109-L114, ISSN: 1040-0605
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- Citations: 43
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