Publications
212 results found
Maynard RL, Donaldson K, Tetley TD, 2013, Type 1 pulmonary epithelial cells: a new compartment involved in the slow phase of particle clearance from alveoli, NANOTOXICOLOGY, Vol: 7, Pages: 350-351, ISSN: 1743-5390
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- Citations: 8
Miragoli M, Novak P, Ruenraroengsak P, et al., 2013, Functional interaction between charged nanoparticles and cardiac tissue: a new paradigm for cardiac arrhythmia?, NANOMEDICINE, Vol: 8, Pages: 725-737, ISSN: 1743-5889
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- Citations: 40
Solomon A, Smyth E, Mitha N, et al., 2013, Induction of platelet aggregation after a direct physical interaction with diesel exhaust particles, JOURNAL OF THROMBOSIS AND HAEMOSTASIS, Vol: 11, Pages: 325-334, ISSN: 1538-7933
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- Citations: 21
Tetley TD, Thorley AJ, 2013, Health effects, Biochemist, Vol: 35, Pages: 14-20, ISSN: 0954-982X
Chen S, Goode AE, Sweeney S, et al., 2013, Sulfidation of silver nanowires inside human alveolar epithelial cells: a potential detoxification mechanism, NANOSCALE, Vol: 5, Pages: 9839-9847, ISSN: 2040-3364
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- Citations: 50
Horwell CJ, Baxter PJ, Hillman SE, et al., 2013, Physicochemical and toxicological profiling of ash from the 2010 and 2011 eruptions of Eyjafjallajokull and Grimsvotn volcanoes, Iceland using a rapid respiratory hazard assessment protocol, Environ Res, Vol: 127, Pages: 63-73, ISSN: 1096-0953
The six week eruption of Eyjafjallajokull volcano in 2010 produced heavy ash fall in a sparsely populated area of southern and south eastern Iceland and disrupted European commercial flights for at least 6 days. We adopted a protocol for the rapid analysis of volcanic ash particles, for the purpose of informing respiratory health risk assessments. Ash collected from deposits underwent a multi-laboratory physicochemical and toxicological investigation of their mineralogical parameters associated with bio-reactivity, and selected in vitro toxicology assays related to pulmonary inflammatory responses. Ash from the eruption of Grimsvotn, Iceland, in 2011 was also studied. The results were benchmarked against ash from Soufriere Hills volcano, Montserrat, which has been extensively studied since the onset of eruptive activity in 1995. For Eyjafjallajokull, the grain size distributions were variable: 2-13 vol% of the bulk samples were <4 microm, with the most explosive phases of the eruption generating abundant respirable particulate matter. In contrast, the Grimsvotn ash was almost uniformly coarse (<3.5 vol%<4 microm material). Surface area ranged from 0.3 to 7.7 m2 g(-1) for Eyjafjallajokull but was very low for Grimsvotn (<0.6 m2 g(-1)). There were few fibre-like particles (which were unrelated to asbestos) and the crystalline silica content was negligible in both eruptions, whereas Soufriere Hills ash was cristobalite-rich with a known potential to cause silicosis. All samples displayed a low ability to deplete lung antioxidant defences, showed little haemolysis and low acute cytotoxicity in human alveolar type-1 like epithelial cells (TT1). However, cell-free tests showed substantial hydroxyl radical generation in the presence of hydrogen peroxide for Grimsvotn samples, as expected for basaltic, Fe-rich ash. Cellular mediators MCP-1, IL-6, and IL-8 showed chronic pro-inflammatory responses in Eyjafjallajokull, Grimsvotn and Soufriere Hills samples, despit
Zambianchi M, Thorley A, Tetley T, 2012, Induction of inflammation, oxidative stress and autophagy in human alveolar type I epithelial cells following exposure to silver nanoparticles, Publisher: EUROPEAN RESPIRATORY SOC JOURNALS LTD, ISSN: 0903-1936
Misra SK, Tetley TD, Thorley AJ, et al., 2012, Engineered Nanomaterials, Pollutants, Human Health and the Environment, Editors: Plant, Ragnarsdottir, Voulvoulis, Voulvoulis, Publisher: Wiley-Blackwell, Pages: 287-318, ISBN: 9780470742600
Derbyshire E, Horwell CJ, Jones TP, et al., 2012, Airborne Particles, Pollutants, Human Health and the Environment: A Risk Based Approach, Pages: 255-286, ISBN: 9780470742617
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- Citations: 4
Jenkins G, Blanchard A, Borok Z, et al., 2012, In search of the fibrotic epithelial cell: opportunities for a collaborative network, THORAX, Vol: 67, Pages: 179-182, ISSN: 0040-6376
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- Citations: 13
Tay A, Nicholson A, von der Thusen J, et al., 2012, Antibody independent micro-filtration biochip for the diagnosis of lung cancer, LUNG CANCER, Vol: 75, Pages: S19-S19, ISSN: 0169-5002
Thorley AJ, Grandolfo D, Lim E, et al., 2011, Innate immune responses to bacterial ligands in the peripheral human lung - role of alveolar epithelial TLR expression and signalling, PLoS One, Vol: 6(7):
Bolasco G, Tracey-White DC, Tolmachova T, et al., 2011, Loss of Rab27 function results in abnormal lung epithelium structure in mice, AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY, Vol: 300, Pages: C466-C476, ISSN: 0363-6143
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- Citations: 13
Ruenraroengsak P, Novak P, Berhanu D, et al., 2011, Respiratory epithelial cytotoxicity and membrane damage (holes) caused by amine-modified nanoparticles., Nanotoxicology, ISSN: 1743-5404
Abstract The respiratory epithelium is a significant target of inhaled, nano-sized particles, the biological reactivity of which will depend on its physicochemical properties. Surface-modified, 50 and 100 nm, polystyrene latex nanoparticles (NPs) were used as model particles to examine the effect of particle size and surface chemistry on transformed human alveolar epithelial type 1-like cells (TT1). Live images of TT1 exposed to amine-modified NPs taken by hopping probe ion conductance microscopy revealed severe damage and holes on cell membranes that were not observed with other types of NPs. This paralleled induction of cell detachment, cytotoxicity and apoptotic (caspase-3/7 and caspase-9) cell death, and increased release of CXCL8 (IL-8). In contrast, unmodified, carboxyl-modified 50 nm NPs and the 100 nm NPs did not cause membrane damage, and were less reactive. Thus, the susceptibility and membrane damage to respiratory epithelium following inhalation of NPs will depend on both surface chemistry (e.g., cationic) and nano-size.
Maher TM, Evans IC, Bottoms SE, et al., 2010, Diminished Prostaglandin E<sub>2</sub> Contributes to the Apoptosis Paradox in Idiopathic Pulmonary Fibrosis, AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, Vol: 182, Pages: 73-82, ISSN: 1073-449X
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- Citations: 142
Swain RJ, Kemp SJ, Goldstraw P, et al., 2010, Assessment of Cell Line Models of Primary Human Cells by Raman Spectral Phenotyping, BIOPHYSICAL JOURNAL, Vol: 98, Pages: 1703-1711, ISSN: 0006-3495
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- Citations: 85
Thorley AJ, Tetley TD, 2010, Mechanisms of uptake of nano-sized latex beads by human alveolar type I epithelial (ATI) cells, 2nd NanoImpactNet Conference
Ruenraroengsak P, Thorley AJ, Tetley TD, 2010, Induction of oxidative stress and cell death in human alveolar epithelium following nanoparticle exposure depends on surface charge, Publisher: AMER THORACIC SOC, ISSN: 1073-449X
Sweeney SS, Ruenraroengsak P, Berhanu D, et al., 2010, Differential reactivity of nano-TiO<sub>2</sub> with human lung alveolar epithelium in vitro: importance of physicochemistry, Publisher: AMER THORACIC SOC, ISSN: 1073-449X
Nuseibeh S, Thorley AJ, Tetley TD, 2010, Effect of serum proteins on the cytotoxic and pro-inflammatory response of human alveolar type I epithelial cells to metal oxide nanoparticles, Publisher: AMER THORACIC SOC, ISSN: 1073-449X
Grandolfo D, Thorley AJ, Salmon GP, et al., 2010, Differential Effect Of Toll-like Receptor Activation On Primary Human Alveolar Epithelium And Alveolar Macrophage Mediator Release In Vitro; Synergistic Effect Of Co-culture, AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, Vol: 181, ISSN: 1073-449X
Berhanu D, Dybowska A, Misra SK, et al., 2009, Characterisation of carbon nanotubes in the context of toxicity studies, Joint Environment and Human Health Programme: Annual Science Day Conference and Workshop, Publisher: BioMed Central, ISSN: 1832-3367
Tsoumakidou M, Kemp SJ, Thorley AJ, et al., 2009, Expression of blood dendritic cell antigens (BDCAs) by CD1a<SUP>+</SUP> human pulmonary cells, RESPIRATORY MEDICINE, Vol: 103, Pages: 935-938, ISSN: 0954-6111
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- Citations: 5
van den Bogaard EHJ, Dailey LA, Thorley AJ, et al., 2009, Inflammatory Response and Barrier Properties of a New Alveolar Type 1-Like Cell Line (TT1), PHARMACEUTICAL RESEARCH, Vol: 26, Pages: 1172-1180, ISSN: 0724-8741
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- Citations: 26
Medford ARL, Douglas SK, Godinho SIH, et al., 2009, Vascular Endothelial Growth Factor (VEGF) isoform expression and activity in human and murine lung injury, Respiratory Research, Vol: 10, ISSN: 1465-993X
BackgroundThe properties of vascular endothelial growth factor (VEGF) as a potent vascular permogen and mitogen have led to investigation of its potential role in lung injury. Alternate spliced VEGF transcript generates several isoforms with potentially differing functions. The purpose of this study was to determine VEGF isoform expression and source in normal and ARDS subjects and investigate the expression and regulation of VEGF isoforms by human alveolar type 2 (ATII) cells.MethodsVEGF protein expression was assessed immunohistochemically in archival normal and ARDS human lung tissue. VEGF isoform mRNA expression was assessed in human and murine lung tissue. Purified ATII cells were cultured with proinflammatory cytokines prior to RNA extraction/cell supernatant sampling/proliferation assay.Measurements and Main ResultsVEGF was expressed on alveolar epithelium, vascular endothelium and alveolar macrophages in normal and ARDS human lung tissue. Increases in VEGF expression were detected in later ARDS in comparison to both normal subjects and early ARDS (p < 0.001). VEGF121, VEGF165 and VEGF189 isoform mRNA expression increased in later ARDS (p < 0.05). The ratio of soluble to cell-associated isoforms was lower in early ARDS than normal subjects and later ARDS and also in murine lung injury. ATII cells constitutionally produced VEGF165 and VEGF121 protein which was increased by LPS (p < 0.05). VEGF165 upregulated ATII cell proliferation (p < 0.001) that was inhibited by soluble VEGF receptor 1 (sflt) (p < 0.05).ConclusionThese data demonstrate that changes in VEGF isoform expression occur in ARDS which may be related to their production by and mitogenic effect on ATII cells; with potentially significant clinical consequences.
Mercer PF, Johns RH, Scotton CJ, et al., 2009, Pulmonary Epithelium Is a Prominent Source of Proteinase-activated Receptor-1-inducible CCL2 in Pulmonary Fibrosis, AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, Vol: 179, Pages: 414-425, ISSN: 1073-449X
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- Citations: 90
BeruBe K, Aufderheide M, Breheny D, et al., 2009, <i>In Vitro</i> Models of Inhalation Toxicity and Disease The Report of a FRAME Workshop, ATLA-ALTERNATIVES TO LABORATORY ANIMALS, Vol: 37, Pages: 89-141, ISSN: 0261-1929
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- Citations: 112
Thorley AJ, Ruenraroengsak P, Tetley TD, 2009, Effect of surface modification of 50nm and 100nm latex particles on uptake by, and viability of, immortal human alveolar type 1-like cells, NanoImpactNet Integrating Conference
Thorley AJ, Tetley TD, 2009, Effect of Physicochemical Properties on Uptake and Cellular Fate of Nanoparticles by Human Alveolar Type I (ATI) Epithelial Cells, American Thoracic Society Annual Meeting
Swain RJ, Kemp SJ, Goldstraw P, et al., 2008, Spectral Monitoring of Surfactant Clearance during Alveolar Epithelial Type II Cell Differentiation, BIOPHYSICAL JOURNAL, Vol: 95, Pages: 5978-5987, ISSN: 0006-3495
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- Citations: 25
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