Publications
78 results found
Jordan S, Evans TW, Burke-Gaffney A, et al., 2000, Toxins associated with gram negative and gram positive bacteria stimulate: IL-8 release from human blood: Implications for ARDS, BRITISH JOURNAL OF PHARMACOLOGY, Vol: 129, Pages: U58-U58, ISSN: 0007-1188
Blease K, Chen Y, Hellewell PG, et al., 1999, Lipoteichoic acid inhibits lipopolysaccharide-induced adhesion molecule expression and IL-8 release in human lung microvascular endothelial cells, JOURNAL OF IMMUNOLOGY, Vol: 163, Pages: 6139-6147, ISSN: 0022-1767
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- Citations: 28
Brooks AVS, Mitchell JA, Evans TW, et al., 1999, Stimulus-specific reduction of neutrophil interleukin-8 release in acute respiratory distress syndrome, THORAX, Vol: 54, Pages: A79-A79, ISSN: 0040-6376
Zhu J, Rogers AV, Burke-Gaffney A, et al., 1999, Cytokine-induced airway epithelial ICAM-1 upregulation: quantification by high-resolution scanning and transmission electron microscopy, EUROPEAN RESPIRATORY JOURNAL, Vol: 13, Pages: 1318-1328, ISSN: 0903-1936
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- Citations: 24
Burke-Gaffney A, Blease K, Hartnell A, et al., 1999, An essential role for VLA-5-fibronectin interaction in TNFα priming of eosinophil adhesion, FASEB JOURNAL, Vol: 13, Pages: A670-A670, ISSN: 0892-6638
Blease K, Chen Y, Hellewell PG, et al., 1998, Interactions between lipoteichoic acid and lipopolysaccharide on human lung microvascular endothelial cell adhesion molecule expression and interleukin-8 release, BRITISH JOURNAL OF PHARMACOLOGY, Vol: 125, Pages: U17-U17, ISSN: 0007-1188
Burke-Gaffney A, Hellewell PG, 1998, Extracellular matrix proteins associated with human bronchial epithelial cells mediate eosinophil adhesion, BRITISH JOURNAL OF PHARMACOLOGY, Vol: 125, Pages: U16-U16, ISSN: 0007-1188
Burke-Gaffney A, Hellewell PG, 1998, A CD18/ICAM-1-dependent pathway mediates eosinophil adhesion to human bronchial epithelial cells, AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY, Vol: 19, Pages: 408-418, ISSN: 1044-1549
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- Citations: 47
Bishop-Bailey D, Burke-Gaffney A, Hellewell PG, et al., 1998, Cyclo-oxygenase-2 regulates inducible ICAM-1 and VCAM-1 expression in human vascular smooth muscle cells, BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, Vol: 249, Pages: 44-47, ISSN: 0006-291X
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- Citations: 41
Blease K, Burke-Gaffney A, Hellewell PG, 1998, Modulation of cell adhesion molecule expression and function on human lung microvascular endothelial cells by inhibition of phosphodiesterases 3 and 4, BRITISH JOURNAL OF PHARMACOLOGY, Vol: 124, Pages: 229-237, ISSN: 0007-1188
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- Citations: 80
Blease K, Seybold J, Adcock IM, et al., 1998, Interleukin-4 and lipopolysaccharide synergize to induce vascular cell adhesion molecule-1 expression in human lung microvascular endothelial cells, AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY, Vol: 18, Pages: 620-630, ISSN: 1044-1549
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- Citations: 38
Blease K, Burke-Gaffney A, Hellewell PG, 1998, Lipoteichoic acid induces cell adhesion molecule expression and IL-8 release from human lung microvascular endothelial cells (HLMVEC)., FASEB JOURNAL, Vol: 12, Pages: A1005-A1005, ISSN: 0892-6638
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- Citations: 1
Burke-Gaffney A, Hellewell PG, 1998, TNFα priming of eosinophil adhesion:: Critical role of β<sub>1</sub>-integrins, FASEB JOURNAL, Vol: 12, Pages: A576-A576, ISSN: 0892-6638
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- Citations: 1
Burke-Gaffney A, Macari DMT, Hellewell PG, 1997, Tumour necrosis factor-α primes eosinophil adhesion to human bronchial epithelial cells, BRITISH JOURNAL OF PHARMACOLOGY, Vol: 122, ISSN: 0007-1188
Burke-Gaffney A, Hellewell PG, 1997, Endogenous nitric oxide limits cytokine-induced damage of murine lung epithelial cells., Am J Physiol, Vol: 272, Pages: L707-L713, ISSN: 0002-9513
This study investigated whether endogenous nitric oxide (NO) limits cytokine-induced damage to the murine lung epithelial cell line LA-4. NO production was assessed as nitrite using the Griess reaction, and cell damage was assessed using ethidium homodimer-1. Cytotoxicity was first detected after a 24-h incubation with a combination of tumor necrosis factor-alpha, interleukin-1beta, and interferon-gamma (cytomix). Nitrite production increased to 78.0 +/- 0.5 nmol/10(6) cells at 24 h. Coincubation of LA-4 with cytomix and NO synthase inhibitors, aminoguanidine (3-1,000 microM) and N(G)-monomethyl-L-arginine (10-1,000 microM), but not N(G)-monomethyl-D-arginine, or a soluble guanylate cyclase inhibitor, 1H-[1,2,4] oxadiazole [4,3-a] quinoxalin-1-one, reduced cytomix-induced nitrite production and increased cytotoxicity up to twofold (24 h). Removal of L-arginine from the medium increased damage; reintroduction of 1,000 microM L-arginine, but not D-arginine, reversed this. In aminoguanidine-treated cells, replacement of NO with an NO donor, S-nitrosoglutathione (30 microM), reversed, in part, the cell damage observed in aminoguanidine/cytomix-treated cells. These results suggest that endogenous NO limits cytokine-induced lung epithelial damage.
Burke-Gaffney A, Hellewell PG, 1996, Tumour necrosis factor-alpha-induced ICAM-1 expression in human vascular endothelial and lung epithelial cells: modulation by tyrosine kinase inhibitors., Br J Pharmacol, Vol: 119, Pages: 1149-1158, ISSN: 0007-1188
1. Tumour necrosis factor-alpha (TNF alpha) increases the expression of the adhesion molecule intercellular adhesion molecule-1 (ICAM-1) on cultured endothelial and epithelial cells and modulation of this may be important in controlling inflammation. Activation of tyrosine kinase(s) is known to be involved in the signal transduction pathways of many cytokines. In this study we have investigated the effects of the tyrosine kinase inhibitors, ST638, tyrphostin AG 1288 and genistein, on TNF alpha-induced ICAM-1 expression in human alveolar epithelial (A549) and vascular endothelial (EAhy926) cell lines and also normal human lung microvascular endothelial cells (HLMVEC). 2. ICAM-1 expression on cultured cells was determined by a sensitive enzyme-linked immunosorbant assay (ELISA). Endothelial or epithelial monolayers were exposed to increasing doses of TNF-alpha (0.01-10 ng ml-1), in the presence or absence of either ST638 (3-100 microM), AG 1288 (3-100 microM) or genistein (100 microM) and ICAM-1 expression was measured at 4 and 24 h. Control experiments examined the effect of ST638 on phorbol 12-myristate 13-acetate (PMA, 20 ng ml-1, 4 h)-stimulated ICAM-1 and compared it to that of a specific protein kinase C inhibitor, R031-8220 (10 microM). Also, functional consequences of changes in ICAM-1 expression were assessed by measuring adhesion of 111 In-labelled human neutrophils to EAhy926 endothelial and A549 epithelial monolayers treated with TNF alpha, in the presence or absence of ST638. 3. ST638 caused a concentration-dependent reduction in TNF alpha- (0.1-10 ng ml-1)-induced ICAM-1 on EAhy926 endothelial (at 4 h) and A549 epithelial monolayers (at 4 and 24 h). In contrast, ST638 caused a concentration-dependent increase in TNF alpha- (0.1-10 ng ml-1)-induced ICAM-1 on EAhy926 endothelial cells at 24 h. Similar effects were seen with AG 1288 or genistein. ST638 (100 microM) significantly (P < 0.01) inhibited ICAM-1 expression on HLMVEC endothelial cells induced b
Burke-Gaffney A, Hellewell PG, 1996, Eotaxin stimulates eosinophil adhesion to human lung microvascular endothelial cells., Biochem Biophys Res Commun, Vol: 227, Pages: 35-40, ISSN: 0006-291X
Effects of the human C-C chemokines eotaxin, MIP-1 alpha, and RANTES on human eosinophil or neutrophil adhesion to human lung microvascular endothelial cells (LMVEC) were investigated. Basal adhesion of unstimulated eosinophils to LMVEC was increased following pretreatment of LMVEC with TNF alpha (10ng/ml) for 6h. Stimulation of eosinophils with eotaxin (30 and 100ng/ml) resulted in increased adhesion to LMVEC pretreated with TNF alpha but not culture medium. Neutrophil adhesion was not increased by eotaxin under similar conditions. Neither MIP-1 alpha (3-100 ng/ml) nor RANTES (3-100 ng/ml) increased eosinophil or neutrophil adhesion to LMVEC pretreated for 6 h with either TNF alpha (10 ng/ml) or culture medium. Monoclonal antibodies (mAb) against eosinophil adhesion molecule VLA-4 (2B4; 30 micrograms/ml) but not CD18 (6.5E; 10 micrograms/ml) inhibited eotaxin-induced eosinophil adhesion to TNF alpha-activated LMVEC. 2B4 in combination with 6.5E reduced adhesion to basal levels. These data show that eotaxin, but not MIP-1 alpha or RANTES, stimulates eosinophil adhesion to LMVEC and that this effect can be abolished by anti-VLA-4 and CD18 mAb in combination. These results suggest that eotaxin may facilitate eosinophil migration from blood vessels in the lung by increasing eosinophil adhesion to endothelial cells.
Burke-Gaffney A, Hellewell PG, 1996, Regulation of ICAM-1 by dexamethasone in a human vascular endothelial cell line EAhy926., Am J Physiol, Vol: 270, Pages: C552-C561, ISSN: 0002-9513
Regulation by dexamethasone of intercellular adhesion molecule-1 (ICAM-1) in cultured monolayers of the human umbilical vein endothelial cell line EAhy926 was investigated. Tumor necrosis factor-alpha (TNF-alpha) and interferon-gamma (IFN-gamma) in combination or lipopolysaccharide (LPS) alone gave time- and dose-dependent increases in ICAM-1. Sustained expression of ICAM-1 was observed after short exposure (30 min) to TNF-alpha + IFN-gamma, but not to LPS. LPS-induced ICAM-1 expression was not inhibited by interleukin-1 (IL-1) receptor antagonist (0.01-100 micrograms/ml). Dexamethasone (1,000 nM) did not inhibit TNF-alpha + IFN-gamma-induced ICAM-1 expression or mRNA induction. In contrast, dexamethasone dose dependently (0.1-1,000 nM) inhibited LPS-induced ICAM-1 expression; however, its effect on mRNA was not established, because ICAM-1 mRNA induced by LPS was not detected at the time points investigated in this study (3 and 20 h). Adhesion of unstimulated human neutrophils to EAhy926 monolayers activated with TNF-alpha + IFN-gamma or LPS was increased in the presence of dexamethasone at low doses, whereas neutrophil adhesion to LPS- but not cytokine-stimulated endothelial cells was significantly reduced (P < 0.05) in the presence of a high dose of dexamethasone (1,000 nM). In conclusion, dexamethasone was demonstrated to regulate the expression and function of ICAM-1 in a stimulus-dependent manner.
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