Imperial College London

ProfessorJaneMitchell

Faculty of MedicineNational Heart & Lung Institute

Professor of Pharmacology in Critical Care Medicine
 
 
 
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Contact

 

+44 (0)20 7351 8137j.a.mitchell

 
 
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Assistant

 

Ms Lisa Quinn +44 (0)20 7594 1345

 
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Location

 

Sir Alexander Fleming BuildingSouth Kensington Campus

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Summary

 

Publications

Publication Type
Year
to

415 results found

Usmani OS, Watson EM, Meah SN, Hodson ME, Mitchell JAet al., 2009, DECLINING RESPIRATORY CLINICAL ACADEMICS: A MODEL FOR REVERSING THE TREND?, Winter Meeting of the British-Thoracic-Society, Publisher: B M J PUBLISHING GROUP, Pages: A165-A166, ISSN: 0040-6376

Conference paper

Armstrong PCJ, Dhanji AA, Tucker AT, Mitchell JA, Warner TDet al., 2009, URINARY 11-DEHYDRO-THROMBOXANE B2 AS A MARKER OF THE ANTI-PLATELET EFFECTS OF CLOPIDOGREL OR ASPIRIN THERAPY IN HEALTHY MALE VOLUNTEERS, Spring Meeting of the British-Society-for-Cardiovascular-Research, Publisher: B M J PUBLISHING GROUP, ISSN: 1355-6037

Conference paper

Ali FY, Hall MG, Desvergne B, Warner TD, Mitchell JAet al., 2009, PPARβ/δ Agonists Modulate Platelet Function via a Mechanism Involving PPAR Receptors and Specific Association/Repression of PKCα-Brief Report, ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, Vol: 29, Pages: 1871-1873, ISSN: 1079-5642

Journal article

Armstrong PCJ, Dhanji A-R, Truss NJ, Zain ZNM, Tucker AT, Mitchell JA, Warner TDet al., 2009, Utility of 96-well plate aggregometry and measurement of thrombi adhesion to determine aspirin and clopidogrel effectiveness, THROMBOSIS AND HAEMOSTASIS, Vol: 102, Pages: 772-778, ISSN: 0340-6245

Journal article

Belvisi MG, Mitchell JA, 2009, Targeting PPAR receptors in the airway for the treatment of inflammatory lung disease, BRITISH JOURNAL OF PHARMACOLOGY, Vol: 158, Pages: 994-1003, ISSN: 0007-1188

Journal article

Mitchell JA, 2009, Oxidative stress by environmental and host derived sources leading to lung inflammation, 46th Congress of the European-Societies-of-Toxicology, Publisher: ELSEVIER IRELAND LTD, Pages: S44-S44, ISSN: 0378-4274

Conference paper

Wort SJ, Ito M, Chou P-C, Mc Master SK, Badiger R, Jazrawi E, de Souza P, Evans TW, Mitchell JA, Pinhu L, Ito K, Adcock IMet al., 2009, Synergistic Induction of Endothelin-1 by Tumor Necrosis Factor α and Interferon γ Is due to Enhanced NF-κB Binding and Histone Acetylation at Specific κB Sites, JOURNAL OF BIOLOGICAL CHEMISTRY, Vol: 284, Pages: 24297-24305

Journal article

Piqueras L, Jesus Sanz M, Perretti M, Morcillo E, Norling L, Mitchell JA, Li Y, Bishop-Bailey Det al., 2009, Activation of PPARβ/δ inhibits leukocyte recruitment, cell adhesion molecule expression, and chemokine release, JOURNAL OF LEUKOCYTE BIOLOGY, Vol: 86, Pages: 115-122, ISSN: 0741-5400

Journal article

Secher T, Vasseur V, Poisson DM, Mitchell JA, Cunha FQ, Alves-Filho JC, Ryffel Bet al., 2009, Crucial Role of TNF Receptors 1 and 2 in the Control of Polymicrobial Sepsis, JOURNAL OF IMMUNOLOGY, Vol: 182, Pages: 7855-7864, ISSN: 0022-1767

Journal article

Ali FY, Armstrong PCJ, Dhanji A-RA, Tucker AT, Paul-Clark MJ, Mitchell JA, Warner TDet al., 2009, Antiplatelet Actions of Statins and Fibrates Are Mediated by PPARs, ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, Vol: 29, Pages: 706-711, ISSN: 1079-5642

Journal article

Paul-Clark MJ, McMaster SK, Sorrentino R, Sriskandan S, Bailey LK, Moreno L, Ryffel B, Quesniaux VF, Mitchell JAet al., 2009, Toll-like Receptor 2 Is Essential for the Sensing of Oxidants during Inflammation, AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, Vol: 179, Pages: 299-306, ISSN: 1073-449X

Journal article

Armstrong PCJ, Truss NJ, Ali FY, Dhanji AA, Vojnovic I, Zain ZNM, Bishop-Bailey D, Paul-Clark MJ, Tucker AT, Mitchell JA, Warner TDet al., 2008, Aspirin and the <i>in vitro</i> linear relationship between thromboxane A<sub>2</sub>-mediated platelet aggregation and platelet production of thromboxane A<sub>2</sub>, JOURNAL OF THROMBOSIS AND HAEMOSTASIS, Vol: 6, Pages: 1933-1943, ISSN: 1538-7933

Journal article

Harrington LS, Lucas R, McMaster SK, Moreno L, Scadding G, Warner TD, Mitchell JAet al., 2008, COX-1, and not COX-2 activity, regulates airway function: relevance to aspirin-sensitive asthma, FASEB JOURNAL, Vol: 22, Pages: 4005-4010, ISSN: 0892-6638

Journal article

Ali FY, Warner TD, Mitchell JA, 2008, Comparison of responses in IP and PPARβ deleted murine platelets, HEART, Vol: 94, ISSN: 1355-6037

Journal article

Zain ZNM, Armstrong PCJ, Pearson NJ, Mitchell JA, Warner TDet al., 2008, Evaluation of aspirin inhibition of platelet aggregation induced by combination of collagen and adrenaline in a 96-well plate format, HEART, Vol: 94, ISSN: 1355-6037

Journal article

Armstrong PCJ, Zain ZNM, Truss NJ, Vojnovic I, Bishop-Bailey D, Mitchell JA, Warner TDet al., 2008, Linear relationship between platelet aggregation and thromboxane A<sub>2</sub> production, HEART, Vol: 94, ISSN: 1355-6037

Journal article

Dhanji AA, Truss NJ, Bishop-Bailey D, Shipolini A, Mitchell JA, Warner TDet al., 2008, Generation of clonal populations of prostaglandin I<sub>2</sub>-producing rat vascular smooth muscle cells:: Potential utility for production of bypass vessels, HEART, Vol: 94, ISSN: 1355-6037

Journal article

Moreno L, McMaster SK, Paul-Clark M, Harrington L, Cartwright N, Secher T, Quesniaux V, Ryffel B, Mitchell JAet al., 2008, The PPAR target gene CD36 is a rate limiting factor for the sensing of gram positive <i>S-aureus</i> in vascular smooth muscle cells but not in macrophages, FUNDAMENTAL & CLINICAL PHARMACOLOGY, Vol: 22, Pages: 48-48, ISSN: 0767-3981

Journal article

Moreno L, Bailey LK, Cartwright N, Paul-Clark M, Mitchell JAet al., 2008, Rip2 mediates NOSII-induction by NOD1 activation in vascular smooth muscle cells but not by TLR4 activation in macrophages, FUNDAMENTAL & CLINICAL PHARMACOLOGY, Vol: 22, Pages: 86-87, ISSN: 0767-3981

Journal article

Sorrentino R, de Souza PM, Sriskandan S, Duffin C, Paul-Clark MJ, Mitchell JAet al., 2008, Pattern recognition receptors and interleukin-8 mediate effects of Gram-positive and Gram-negative bacteria on lung epithelial cell function, BRITISH JOURNAL OF PHARMACOLOGY, Vol: 154, Pages: 864-871, ISSN: 0007-1188

Journal article

Issa R, Sorrentino R, Sukkar MB, Sriskandan S, Chung KF, Mitchell JAet al., 2008, Differential regulation of CCL-II/eotaxin-I and CXCL-8/IL-8 by Gram-positive and Gram-negative bacteria in human airway smooth muscle cells, Respiratory Research, Vol: 9, ISSN: 1465-993X

Background: Bacterial infections are a cause of exacerbation of airway disease. Airway smoothmuscle cells (ASMC) are a source of inflammatory cytokines/chemokines that may propagate localairway inflammatory responses. We hypothesize that bacteria and bacterial products could inducecytokine/chemokine release from ASMC.Methods: Human ASMC were grown in culture and treated with whole bacteria or pathogenassociated molecular patterns (PAMPs) for 24 or 48 h. The release of eotaxin-1, CXCL-8 orGMCSF was measured by ELISA.Results: Gram-negative E. coli or Gram-positive S. aureus increased the release of CXCL-8, as didIL-1β, LPS, FSL-1 and Pam3CSK4, whereas FK565, MODLys18 or Poly I:C did not. E. coli inhibitedeotaxin-1 release under control conditions and after stimulation with IL-1β. S. aureus tended toinhibit eotaxin-1 release stimulated with IL-1β. E. coli or LPS, but not S. aureus, induced the releaseof GMCSF.Conclusion: Gram-positive or Gram-negative bacteria activate human ASMC to release CXCL-8.By contrast Gram-negative bacteria inhibited the release of eotaxin-1 from human ASMCs. E. coli,but not S. aureus induced GMCSF release from cells.Our findings that ASMC can respond directly to Gram-negative and Gram-positive bacteria byreleasing the neutrophil selective chemokine, CXCL-8, is consistent with what we know about therole of neutrophil recruitment in bacterial infections in the lung. Our findings that bacteria inhibitthe release of the eosinophil selective chemokine, eotaxin-1 may help to explain the mechanismsby which bacterial immunotherapy reduces allergic inflammation in the lung.

Journal article

McMaster SK, Paul-Clark MJ, Walters M, Fleet M, Anandarajah J, Sriskandan S, Mitchell JAet al., 2008, Cigarette smoke inhibits macrophage sensing of Gram-negative bacteria and lipopolysaccharide: relative roles of nicotine and oxidant stress, BRITISH JOURNAL OF PHARMACOLOGY, Vol: 153, Pages: 536-543, ISSN: 0007-1188

Journal article

Paul-Clark MJ, Sorrentino R, Bailey LK, Sriskandan S, Mitchell JAet al., 2008, Gram-positive and gram-negative bacteria synergize with oxidants to release CXCL8 from innate immune cells, MOLECULAR MEDICINE, Vol: 14, Pages: 238-246, ISSN: 1076-1551

Journal article

Warner TD, Mitchell JA, 2008, COX-2 selectivity alone does not define the cardiovascular risks associated with non-steroidal anti-inflammatory drugs, LANCET, Vol: 371, Pages: 270-273, ISSN: 0140-6736

Journal article

Mitchell JA, Ali F, Bailey L, Moreno L, Harrington LSet al., 2008, Role of nitric oxide and prostacyclin as vasoactive hormones released by the endothelium, EXPERIMENTAL PHYSIOLOGY, Vol: 93, Pages: 141-147, ISSN: 0958-0670

Journal article

Mitchell JA, Ali F, Bailey L, Moreno L, Harrington LSet al., 2008, Role of nitric oxide and prostacyclin as vasoactive hormones released by the endothelium, Life Science Conference 2007, Pages: 141-147

The endothelium lines the luminal surface of every blood vessel, allowing it contact with circulating blood elements, as well as the underlying vascular smooth muscle layer. In healthy vessels, the endothelium expresses constitutive forms of nitric oxide synthase (NOSIII) and cyclo-oxygenase (COX-1), which produce the vasoactive hormones NO and prostacyclin, respectively. Both NO and prostacyclin relax blood vessels and inhibit platelet activation. The actions of prostacyclin are mediated by cell surface prostacyclin (IP) receptors and/or intracellular peroxisome proliferator-activated receptors (PPAR)beta. The actions of NO are mediated predominately by activation of intracellular guanylyl cyclase, leading to the formation of cGMP. In platelets, the actions of NO and prostacyclin are synergistic, but in vessels their actions are additive. In diseased vessels, inducible forms of NOS (NOSII) and cyclo-oxygeanse (COX-2) are expressed in vascular smooth muscle, resulting in the release of large amounts of NO, prostacyclin and prostaglandin E-2. The relative contribution of NOSII and COX-2 to vascular inflammation is still debated, but is likely to result in both protective and damaging responses. The relative contribution of constitutive forms of NOS and COX, as well as interactions between IP, PPAR beta and guanylyl cyclase pathways in vessels and platelets, is discussed.

Conference paper

Oltmanns U, Walters M, Sukkar M, Xie S, Issa R, Mitchell J, Johnson M, Chung KFet al., 2008, Fluticasone, but not salmeterol, reduces cigarette smoke-induced production of interleukin-8 in human airway smooth muscle, PULMONARY PHARMACOLOGY & THERAPEUTICS, Vol: 21, Pages: 292-297, ISSN: 1094-5539

Journal article

Harrington LS, Belcher E, Moreno L, Carrier MJ, Mitchell JAet al., 2007, Homeostatic role of toll-like receptor 4 in the endothelioum and heart, JOURNAL OF CARDIOVASCULAR PHARMACOLOGY AND THERAPEUTICS, Vol: 12, Pages: 322-326, ISSN: 1074-2484

Journal article

Mitchell JA, Ryffel B, Quesniaux VFJ, Cartwright N, Paul-Clark Met al., 2007, Role of pattern-recognition receptors in cardiovascular health and disease, BIOCHEMICAL SOCIETY TRANSACTIONS, Vol: 35, Pages: 1449-1452, ISSN: 0300-5127

Journal article

Harrington LS, Evans RJ, Wray J, Norling L, Swales KE, Vial C, Ali F, Carrier MJ, Mitchell JAet al., 2007, Purinergic 2X<sub>1</sub> receptors mediate endothelial dependent vasodilation to ATP, MOLECULAR PHARMACOLOGY, Vol: 72, Pages: 1132-1136, ISSN: 0026-895X

Journal article

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