Publications
18 results found
Selway IL, Seldon PM, Harikumar P, et al., 2011, Differentially-expressed genes identified from patients with Langerhans Cell Histiocytosis, Annual Meeting of the Society-for-Investigative-Dermatology, Publisher: NATURE PUBLISHING GROUP, Pages: S15-S15, ISSN: 0022-202X
Walsh E, Seldon PM, 2009, Establishing the positive impact of Roberts developmennt activities on completing doctoral students:variation by gender and domicile, Vitae researcher development conference 2009: realising the potential of researchers
Seaton ED, Mouser PE, Charakida A, et al., 2006, Investigation of the mechanism of action of nonablative pulsed-dye laser therapy in photorejuvenation and inflammatory acne vulgaris, BRITISH JOURNAL OF DERMATOLOGY, Vol: 155, Pages: 748-755, ISSN: 0007-0963
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- Citations: 60
Seldon PM, Gueniche A, Breton L, et al., 2006, Effect of elastase inhibitor N-Acetyl-N-[3-( trifl uoromethyl) phenyl] valylglycine) on langerhans cell function and cytokine generation, 36th Annual Meeting of the European-Society-of-Dermatology-Research (ESDR), Publisher: NATURE PUBLISHING GROUP, Pages: 54-54, ISSN: 0022-202X
Seaton E, Charikida A, Seldon P, et al., 2005, Investigation of the mechanism of nonablative pulsed-dye laser therapy in acne vulgaris and photorejuvenation, 63rd Annual Meeting of the American-Academy-of-Dermatology, Publisher: MOSBY, INC, Pages: P3-P3, ISSN: 0190-9622
Seldon PM, Meja KK, Giembycz MA, 2005, Rolipram, salbutamol and prostaglandin E-2 suppress TNF alpha release from human monocytes by activating Type II cAMP-dependent protein kinase, PULMONARY PHARMACOLOGY & THERAPEUTICS, Vol: 18, Pages: 277-284, ISSN: 1094-5539
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- Citations: 14
Mouser P, Seldon P, Seaton E, et al., 2004, Chemakine MRNA expression in acne vulgaris, 65th Annual Meeting of the Society-for-Investigative-Dermatology, Publisher: BLACKWELL PUBLISHING INC, Pages: A129-A129, ISSN: 0022-202X
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- Citations: 1
Seldon PM, Giembycz MA, 2001, Suppression of granulocyte/macrophage colony-stimulating factor release from human monocytes by cyclic AMP-elevating drugs: role of interleukin-10, BRITISH JOURNAL OF PHARMACOLOGY, Vol: 134, Pages: 58-67, ISSN: 0007-1188
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- Citations: 21
Meja KK, Seldon PM, Nasuhara Y, et al., 2000, p38 MAP kinase and MKK-1 co-operate in the generation of GM-CSF from LPS-stimulated human monocytes by an NF-kappa B-independent mechanism, BRITISH JOURNAL OF PHARMACOLOGY, Vol: 131, Pages: 1143-1153, ISSN: 0007-1188
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- Citations: 59
Seldon PM, Stevens DA, Adcock IM, et al., 1998, Albuterol does not antagonize the inhibitory effect of dexamethasone on monocyte cytokine release, AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, Vol: 157, Pages: 803-809, ISSN: 1073-449X
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- Citations: 16
Seldon PM, Stevens DA, Adcock IM, et al., 1998, Albuterol does not antagonize the inhibitory effect of dexamethasone on monocyte cytokine release, American Journal of Respiratory and Critical Care Medicine, Vol: 157, Pages: 803-809, ISSN: 1073-449X
β2-Adrenoceptor agonists given by the inhaled route are the most effective bronchodilators known, yet high doses of these drugs may be associated with an increase in asthma mortality and morbidity. One theory for this paradox is that chronic use of β2-adrenoceptor agonists compromises the antiinflammatory action of glucocorticosteroids. This hypothesis derives from the ability of albuterol and fenoterol to inhibit the interaction of the glucocorticosteroid receptor (GR) with proinflammatory transcriptional activators acting on the promoter region of certain target genes that encode cytokines such as tumor necrosis factor-α (TNFα) and granulocyte/macrophage colony-stimulating factor (GM-CSF). However, the functional relevance of these results has not been formally investigated. We have tested the hypothesis that albuterol reduces the ability of dexamethasone to inhibit the generation of TNFα and GM-CSF from lipopolysaccharide (LPS)-stimulated human monocytes. Pretreatment of human monocytes with albuterol (1 and 100 μM) for 5 and for 180 min inhibited maximally TNFα generation by approximately 25%. However, regardless of the concentration of albuterol, or the time of preincubation, the inhibitory effect of dexamethasone was not significantly affected with respect to the EC50 or the maximal effect produced. Qualitatively identical data were obtained when GM-CSF release was used as an index of monocyte activation. We conclude that high concentrations of albuterol do not compromise the ability of dexamethasone to suppress the Generation of TNFα and GM-CSF from LPS-stimulated human monocytes.
Seldon PM, Barnes PJ, Giembycz MA, 1998, Interleukin-10 does not mediate the inhibitory effect of PDE-4 inhibitors and other cAMP-elevating drugs on lipopolysaccharide-induced tumors necrosis factor-alpha generation from human peripheral blood monocytes., Cell Biochem Biophys, Vol: 29, Pages: 179-201, ISSN: 1085-9195
Lipopolysaccharide (LPS)-induced liver injury in mice and LPS-induced tumor necrosis factor-alpha (TNF-alpha) generation by murine macrophages and hepatocytes are suppressed markedly by agents that elevate intracellular cAMP. Phosphodiesterase (PDE)-4 inhibitors, beta 2-adrenoceptor agonists, and E-series prostaglandins also attenuate the induction of the TNF-alpha gene in human monocytes in response to bacterial LPS. The mechanism of action of cAMP is unclear, but in the mouse, is believed to involve the generation of this anti-inflammatory cytokine, interleukin-10 (IL-10). In this article, we describe the results of studies designed to determine the extent to which IL-10 contributes to the suppression of TNF-alpha generation from LPS-stimulated human monocytes evoked by 8-bromo cyclic AMP (8-Br-cAMP), rolipram, salbutamol, and prostaglandin E2 (PGE2). LPS evoked a time- and concentration-dependent generation of TNF-alpha (t1/2 = 4.5 h; EC50 = 273 pg/mL), which was inhibited by exogenous human recombinant (h) IL-10 (IC50 = 124 pg/mL), and by rolipram (EC50 = 420 nM), 8-Br-cAMP (EC50 = 77 (microM), PGE2 (EC50 = 15 nM) and salbutamol (EC50 = 20 nM). In addition, 8-Br-cAMP, PGE2; and salbutamol (but not rolipram) augmented significantly LPS-induced IL-10 production (two-to-fivefold) under identical experimental conditions. Pretreatment of monocytes with an anti-IL-10 monoclonal antibody (MAb) that abolished the inhibitory action of a maximally effective concentration of exogenous hrIL-10, failed to attenuate the inhibitory effect of rolipram, PGE2, salbutamol, and 8-Br-cAMP. Anti-IL-10 was similarly inactive when the number of monocytes seeded was increased from 0.5 to 4 x 10(6)/mL or when measurements were made at 42 h post-LPS, a time when the concentration of IL-10 released was maximal. Collectively, these data suggest that in contrast to murine hepatocytes and macrophages, IL-10 does not mediate the inhibitory effect of cAMP-elevating drugs on TNF-alpha generation
Saunders MA, Mitchell JA, Seldon PM, et al., 1997, Release of granulocyte-macrophage colony stimulating factor by human cultured airway smooth muscle cells: Suppression by dexamethasone, BRITISH JOURNAL OF PHARMACOLOGY, Vol: 120, Pages: 545-546, ISSN: 0007-1188
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- Citations: 106
Meja K, Seldon PM, Barnes PJ, et al., 1996, Characterisation of the prostanoid receptors that mediate inhibition of lipopolysaccharide-induced tumour necrosis factor-alpha generation from human monocytes, BRITISH JOURNAL OF PHARMACOLOGY, Vol: 119, Pages: P158-P158, ISSN: 0007-1188
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- Citations: 1
Seldon PM, Barnes PJ, Giembycz MA, 1996, The inhibitory effect of cyclic AMP-elevating drugs on LPS-induced TNF alpha generation from human monocytes is not mediated by IL-10, BRITISH JOURNAL OF PHARMACOLOGY, Vol: 119, Pages: P159-P159, ISSN: 0007-1188
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- Citations: 1
SELDON PM, BARNES PJ, MEJA K, et al., 1995, SUPPRESSION OF LIPOPOLYSACCHARIDE-INDUCED TUMOR-NECROSIS-FACTOR-ALPHA GENERATION FROM HUMAN PERIPHERAL-BLOOD MONOCYTES BY INHIBITORS OF PHOSPHODIESTERASE-4 - INTERACTION WITH STIMULANTS OF ADENYLYL-CYCLASE, MOLECULAR PHARMACOLOGY, Vol: 48, Pages: 747-757, ISSN: 0026-895X
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- Citations: 121
SELDON PM, BARNES PJ, GIEMBYCZ MA, 1994, PHOSPHODIESTERASE-IV INHIBITORS AND BETA-ADRENOCEPTOR AGONISTS SUPPRESS LIPOPOLYSACCHARIDE-INDUCED TUMOR-NECROSIS-FACTOR-ALPHA GENERATION BY HUMAN PERIPHERAL-BLOOD MONOCYTES, BRITISH JOURNAL OF PHARMACOLOGY, Vol: 112, Pages: U110-U110, ISSN: 0007-1188
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- Citations: 1
RING PC, SELDON PM, BARNES PJ, et al., 1993, PHARMACOLOGICAL CHARACTERIZATION OF A RECEPTOR FOR PLATELET-ACTIVATING-FACTOR ON GUINEA-PIG PERITONEAL-MACROPHAGES USING [H-3] APAFANT, A SELECTIVE AND COMPETITIVE PLATELET-ACTIVATING-FACTOR ANTAGONIST - EVIDENCE THAT THE NONCOMPETITIVE BEHAVIOR OF APAFANT IN FUNCTIONAL-STUDIES RELATES TO SLOW KINETICS OF DISSOCIATION, MOLECULAR PHARMACOLOGY, Vol: 43, Pages: 302-312, ISSN: 0026-895X
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- Citations: 8
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