Publications
221 results found
Sanz MJ, Ponath PD, Mackay CR, et al., 1998, Human eotaxin induces α and β<sub>2</sub> integrin-dependent eosinophil accumulation in rat skin in vivo:: Delayed generation of eotaxin in response to IL-4, JOURNAL OF IMMUNOLOGY, Vol: 160, Pages: 3569-3576, ISSN: 0022-1767
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- Citations: 45
Mitchell JA, Bishop-Bailey D, Evans TW, et al., 1998, Release of neutrophil activating cytokines by human arterial and venous smooth muscle cells, BRITISH JOURNAL OF PHARMACOLOGY, Vol: 123, Pages: U56-U56, ISSN: 0007-1188
Au BT, Teixeira MM, Collins PD, et al., 1998, Effect of PDE4 inhibitors on zymosan-induced IL-8 release from human neutrophils: Synergism with prostanoids and salbutamol, BRITISH JOURNAL OF PHARMACOLOGY, Vol: 123, Pages: 1260-1266, ISSN: 0007-1188
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- Citations: 58
Alcamà A, Symons JA, Collins PD, et al., 1998, Blockade of chemokine activity by a soluble chemokine binding protein from vaccinia virus, JOURNAL OF IMMUNOLOGY, Vol: 160, Pages: 624-633, ISSN: 0022-1767
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- Citations: 218
Williams CMM, Newton DJ, Wilson SA, et al., 1998, Conserved structure and tissue expression of rat eotaxin, IMMUNOGENETICS, Vol: 47, Pages: 178-180, ISSN: 0093-7711
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- Citations: 24
Conroy DM, Humbles AA, Rankin SM, et al., 1997, The role of the eosinophil-selective chemokine, eotaxin, in allergic and non-allergic airways inflammation, MEMORIAS DO INSTITUTO OSWALDO CRUZ, Vol: 92, Pages: 183-191, ISSN: 0074-0276
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- Citations: 25
Teixeira MM, Williams TJ, Hellewell PG, 1997, Description of an in vivo model for the assessment of eosinophil chemoattractants in the mouse, MEMORIAS DO INSTITUTO OSWALDO CRUZ, Vol: 92, Pages: 211-214, ISSN: 0074-0276
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- Citations: 4
Ying S, Robinson DS, Meng Q, et al., 1997, Enhanced expression of eotaxin and CCR3 mRNA and protein in atopic asthma. Association with airway hyperresponsiveness and predominant colocalization of eotaxin mRNA to bronchial epithelial and endothelial cells, EUROPEAN JOURNAL OF IMMUNOLOGY, Vol: 27, Pages: 3507-3516, ISSN: 0014-2980
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- Citations: 364
Boshoff C, Endo Y, Collins PD, et al., 1997, Angiogenic and HIV-inhibitory functions of KSHV-encoded chemokines, SCIENCE, Vol: 278, Pages: 290-294, ISSN: 0036-8075
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- Citations: 398
Teixeira MM, Wells TNC, Lukacs NW, et al., 1997, Chemokine-induced eosinophil recruitment - Evidence of a role for endogenous eotaxin in an in vivo allergy model in mouse skin, JOURNAL OF CLINICAL INVESTIGATION, Vol: 100, Pages: 1657-1666, ISSN: 0021-9738
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- Citations: 142
Li D, Wang D, GriffithsJohnson DA, et al., 1997, Eotaxin protein and gene expression in guinea-pig lungs: constitutive expression and upregulation after allergen challenge, EUROPEAN RESPIRATORY JOURNAL, Vol: 10, Pages: 1946-1954, ISSN: 0903-1936
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- Citations: 61
Humbles AA, Conroy DM, Marleau S, et al., 1997, Kinetics of eotaxin generation and its relationship to eosinophil accumulation in allergic airways disease: Analysis in a guinea pig model in vivo, JOURNAL OF EXPERIMENTAL MEDICINE, Vol: 186, Pages: 601-612, ISSN: 0022-1007
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- Citations: 212
Mitchell JA, Williams FM, Williams TJ, et al., 1997, Role of nitric oxide in the dilator actions of capsaicin-sensitive nerves in the rabbit coronary circulation., Neuropeptides, Vol: 31, Pages: 333-338, ISSN: 0143-4179
Perivascular sensory nerves release calcitonin gene-related peptide (CGRP) and substance P, the dilator actions of which can be regulated by nitric oxide (NO). This study investigated the role of NO in the vasodilation caused by sensory nerve stimulation, by capsaicin, or exogenous CGRP and substance P in the isolated perfused coronary circulation of the rabbit. Coronary perfusion pressure (CPP) was raised in order to observe vasodilator responses, using the thromboxane mimetic, U46619. Capsaicin (3 x 10(-6) moles), alpha CGRP (3 x 10(-11) moles) and substance P (3 x 10(-12) moles) caused comparable reductions in CCP. At these concentrations, responses to capsaicin and CGRP were inhibited by the antagonist CGRP(8-37) but unaffected by the neurokinin-1 receptor antagonist, CP 96,345. The nitric oxide synthase inhibitor, NG nitro L-arginine methyl ester inhibited the effects of substance P and capsaicin but not CGRP. These results suggest that CGRP release following capsaicin-induced sensory nerve activation is modulated by NO.
Norman KE, Williams TJ, Rossi AG, 1997, Comparison of the reversed passive Arthus and local Shwartzman reactions of rabbit skin: Effects of the long-acting PAF antagonist UM-74,505, BRITISH JOURNAL OF PHARMACOLOGY, Vol: 120, Pages: 1286-1293, ISSN: 0007-1188
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- Citations: 5
Stellato C, Collins P, Ponath PD, et al., 1997, Production of the novel C-C chemokine MCP-4 by airway cells and comparison of its biological activity to other C-C chemokines., J Clin Invest, Vol: 99, Pages: 926-936, ISSN: 0021-9738
Monocyte chemotactic protein-4 (MCP-4) is a newly identified C-C chemokine with potent eosinophil chemoattractant properties. We describe studies of its biological activity in vitro to induce chemotaxis of peripheral blood eosinophils and to induce histamine release from IL-3-primed peripheral blood basophils. MCP-4 and eotaxin caused a similar rise in eosinophil intracytoplasmic Ca2+ and complete cross-desensitization. MCP-4 also abolished the eosinophil Ca2+ response to MCP-3 and partially desensitized the response to macrophage inflammatory protein-1alpha. MCP-4 activated cell migration via either CCR2b or CCR3 in mouse lymphoma cells transfected with these chemokine receptors. MCP-4 inhibited binding of 125I-eotaxin to eosinophils and CCR3-transfected cells and inhibited 125I-MCP-1 binding to CCR2b-transfectants. MCP-4 mRNA was found in cells collected in bronchoalveolar lavage of asthmatic and nonasthmatic subjects and was prominently expressed in human lung and heart. MCP-4 mRNA was expressed in several human bronchial epithelial cell lines after cytokine stimulation. Pretreatment of BEAS-2B epithelial cells with the glucocorticoid budesonide inhibited MCP-4 mRNA expression. These features make MCP-4 a candidate for playing a role in eosinophil recruitment during allergic respiratory diseases.
Sabroe I, Williams TJ, Hebert CA, et al., 1997, Chemoattractant cross-desensitization of the human neutrophil IL-8 receptor involves receptor internalization and differential receptor subtype regulation, JOURNAL OF IMMUNOLOGY, Vol: 158, Pages: 1361-1369, ISSN: 0022-1767
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- Citations: 99
Rajakulasingam K, Hamid Q, OBrien F, et al., 1997, RANTES in human allergen-induced rhinitis - Cellular source and relation to tissue eosinophilia, AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, Vol: 155, Pages: 696-703, ISSN: 1073-449X
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- Citations: 49
GriffithsJohnson DA, Collins PD, Jose PJ, et al., 1997, Animal models of asthma: Role of chemokines, CHEMOKINE RECEPTORS, Vol: 288, Pages: 241-266, ISSN: 0076-6879
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- Citations: 27
Sabroe I, Hébert CA, Williams TJ, et al., 1996, Cross-desensitisation of neutrophil IL-8 receptors involves differential receptor subtype regulation, Thorax, Vol: 51, ISSN: 0040-6376
Human neutrophil IL-8 receptors (IL-8R) undergo rapid homologous desensitisation following repeated stimulation with IL-8. It has also been demonstrated that cross-desensitisation of IL-8R may occur after stimulation with C5a or fMLP (Richardson et al; J.Biol.Chem:270:27829). We investigated the underlying mechanisms of this cross-desensitisation response to IL-8 induced by pretreatment with fMLP or C5a. We used a combination of 125I-IL-8 binding studies and flow cytometry with specific anti-IL-8R subtype antibodies to measure IL-8R surface expression. We found the cross-desensitisation induced by fMLP or C5a was associated with a subsequent reduction in IL-8R on the surface of neutrophils. The reduction in IL-8R number following cross-desensitisation was not reversed on removal of the C5a or fMLP stimulus. FACS analysis showed that this heterologous desensitisation resulted from a pronounced and sustained downregulation of IL-8RB only. Calcium mobilisation studies using melanoma growth stimulatory activity (MGSA) and IL-8 suggests that a sustained loss of IL-8RB may play a part in maintaining fMLP-induced IL-8R cross-desensitisation. In vivo, C5a is generated in the first phase of an inflammatory reaction, followed by a later phase of IL-8 generation, mostly from neutrophils (Collins et al; J.Immunol: 146:677). Therefore chemoattractant-induced neutrophil cross-desensitisation may be of importance in regulating neutrophil accumulation during the inflammatory response in vivo, and may be mediated predominantly by IL-8RB.
Marleau S, GriffithsJohnson DA, Collins PD, et al., 1996, Human RANTES acts as a receptor antagonist for guinea pig eotaxin in vitro and in vivo, JOURNAL OF IMMUNOLOGY, Vol: 157, Pages: 4141-4146, ISSN: 0022-1767
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- Citations: 18
Wakelin MW, Sanz MJ, Dewar A, et al., 1996, An anti-platelet-endothelial cell adhesion molecule-1 antibody inhibits leukocyte extravasation from mesenteric microvessels in vivo by blocking the passage through the basement membrane, Journal of Experimental Medicine, Vol: 184, Pages: 229-239, ISSN: 1540-9538
Platelet-endothelial cell adhesion molecule-1 (PECAM-1, CD31) plays an active role in theprocess of leukocyte migration through cultured endothelial cells in vitro and anti-PECAM-1antibodies (Abs) inhibit accumulation ofleukocytes into sites of inflammation in vivo. Despitethe latter, it is still not clear at which stage of leukocyte emigration in vivo PECAM-1 is involved.To address this point directly, we studied the effect of an anti-PECAM-1 Ab, recognizingrat PECAM-1, on leukocyte responses within rat mesenteric microvessels using intravitalmicroscopy. In mesenteric preparations activated by interleukin (IL)-113, the anti-PECAM-1Ab had no significant effect on the rolling or adhesion ofleukocytes, but inhibited their migrationinto the surrounding extravascular tissue in a dose-dependent manner. Although in somevessel segments these leukocytes had come to a halt within the vascular lumen, often the leukocytesappeared to be trapped within the vessel wall. Analysis of these sections by electron microscopyrevealed that the leukocytes had passed through endothelial cell junctions but not thebasement membrane. In contrast to the effect of the Ab in mesenteric preparations treated withIL-113, leukocyte extravasation induced by topical or intraperitoneal administration of thechemotactic peptide formyl-methionyl-leucyl-phenylalanine was not inhibited by the antiPECAM-1Ab. These results directly demonstrate a role for PECAM-1 in leukocyte extravasationin vivo and indicate that this involvement is selective for leukocyte extravasation elicitedby certain inflammatory mediators. Further, our findings provide the first in vivo indicationthat PECAM-1 may have an important role in triggering the passage of leukocytes through theperivascular basement membrane.
Fallon PG, Teixeira MM, Neice CM, et al., 1996, Enhancement of Schistosoma mansoni infectivity by intradermal injections of larval extracts: A putative role for larval proteases, JOURNAL OF INFECTIOUS DISEASES, Vol: 173, Pages: 1460-1466, ISSN: 0022-1899
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- Citations: 14
Teixeira MM, Williams TJ, Hellewell PG, 1996, Effects of dexamethasone and cyclosporin A on the accumulation of eosinophils in acute cutaneous inflammation in the guinea-pig, BRITISH JOURNAL OF PHARMACOLOGY, Vol: 118, Pages: 317-324, ISSN: 0007-1188
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- Citations: 12
Saunders MA, Mitchell JA, HIrst SJ, et al., 1996, Characterisation of cyclo-oxygenase-2 induction in human airway smooth muscle cells, BRITISH JOURNAL OF PHARMACOLOGY, Vol: 117, Pages: P82-P82, ISSN: 0007-1188
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- Citations: 1
Miotla JM, Williams TJ, Hellewell PG, et al., 1996, Role for the beta(2) integrin CD11b in mediating experimental lung injury in mice, AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY, Vol: 14, Pages: 363-373, ISSN: 1044-1549
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- Citations: 27
Norman KE, Williams TJ, Feldmann M, et al., 1996, Effect of soluble P55 tumour-necrosis factor binding fusion protein on the local Shwartzman and Arthus reactions., Br J Pharmacol, Vol: 117, Pages: 471-478, ISSN: 0007-1188
1. In this study, the effects of a protein synthesis inhibitor, cycloheximide, and a soluble tumour necrosis factor (TNF) binding/IgG fusion protein, p55-sf2, on the priming and challenge stages of the local Shwartzman reaction (LSR) were assessed and compared with their effects on the acute inflammatory response induced by recombinant human tumour necrosis factor-alpha (rhTNF), lipopolysaccharide (LPS) and a reversed passive Arthus (RPA) reaction in rabbit skin. 2. The LSR was induced in skin by giving an intradermal (i.d.) priming injection of LPS followed by two i.v. challenge injections 20 h and 22 h later. Accumulation of 51-Cr-labelled red blood cells and [125I]-albumin were measured at 24 h as markers of haemorrhage and oedema formation, respectively. 3. The RPA reaction was induced in the rabbit by giving i.d. injections of Arthus anti-serum (anti-bovine-gamma-globulin, BGG) followed 5 min later by an i.v. injection of the antigen (BGG). Oedema formation and the accumulation of 111In-labelled neutrophils produced in the RPA reaction and in response to i.d. injection of rhTNF and LPS were measured over the 4 h period after inducing the responses. 4. A single local injection of cycloheximide (10 micrograms/site) did not inhibit neutrophil accumulation or oedema formation produced by 100% Arthus anti-sera. Although LPS injected i.d. induced a marked dose-dependent neutrophil accumulation, there was little associated plasma leakage. Cycloheximide (10 micrograms/site) did not significantly inhibit the neutrophil accumulation induced by LPS (0.1 microgram/site). In the LSR, priming i.d. injections of LPS caused a dose-dependent increase in haemorrhage and plasma leakage at skin sites after challenge with LPS (two injections of 100 micrograms, i.v.). Co-injection of a single dose of cycloheximide (10 micrograms/site) with LPS (30 micrograms/site) caused a marked reduction in the amount of haemorrhage. Local cycloheximide (10 micrograms/site) administered immediatel
Teixeira MM, Williams TJ, Hellewell PG, 1995, Mechanisms and pharmacological manipulation of eosinophil accumulation in vivo, TRENDS IN PHARMACOLOGICAL SCIENCES, Vol: 16, Pages: 418-423, ISSN: 0165-6147
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- Citations: 60
NOURSHARGH S, WILLIAMS TJ, 1995, MOLECULAR AND CELLULAR INTERACTIONS MEDIATING GRANULOCYTE ACCUMULATION IN-VIVO, SEMINARS IN CELL BIOLOGY, Vol: 6, Pages: 317-326, ISSN: 1043-4682
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- Citations: 5
Mitchell JA, Larkin S, Williams TJ, 1995, Cyclooxygenase-2: regulation and relevance in inflammation., Biochem Pharmacol, Vol: 50, Pages: 1535-1542, ISSN: 0006-2952
Collins PD, Marleau S, Griffiths-Johnson DA, et al., 1995, Cooperation between interleukin-5 and the chemokine eotaxin to induce eosinophil accumulation in vivo., Journal of Experimental Medicine, Vol: 182, Pages: 1169-1174, ISSN: 1540-9538
Experiments were designed to study the effect of systemically administered IL-5 on local eosinophil accumulation induced by the intradermal injection of the chemokine eotaxin in the guinea pig. Intravenous interleukin-5 (IL-5) stimulated a rapid and dramatic increase in the numbers of accumulating eosinophils induced by i.d.-injected eotaxin and, for comparison, leukotriene B4. The numbers of locally accumulating eosinophils correlated directly with a rapid increase in circulating eosinophils: circulating eosinophil numbers were 13-fold higher 1 h after intravenous IL-5 (18.3 pmol/kg). This increase in circulating cells corresponded with a reduction in the number of displaceable eosinophils recovered after flushing out the femur bone marrow cavity. Intradermal IL-5, at the doses tested, did not induce significant eosinophil accumulation. We propose that these experiments simulate important early features of the tissue response to local allergen exposure in a sensitized individual, with eosinophil chemoattractant chemokines having an important local role in eosinophil recruitment from blood microvessels, and IL-5 facilitating this process by acting remotely as a hormone to stimulate the release into the circulation of a rapidly mobilizable pool of bone marrow eosinophils. This action of IL-5 would be complementary to the other established activities of IL-5 that operate over a longer time course.
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