Professor Takata holds the Sir Ivan Magill Chair in Anaesthetics at Imperial College London. He is Professor of Molecular Physiology in Critical Care, and Head of the Section of Anaesthetics, Pain Medicine & Intensive Care within the Department of Surgery & Cancer. He is also an Honorary Consultant in Anaesthesia & Intensive Care at the Chelsea & Westminster Hospital.
Professor Takata was originally trained as a paediatric anaesthetist/intensivist in Japan and Canada. He obtained a broad range of research training spanning from respiratory physiology at Johns Hopkins, molecular biology at Harvard, to immunology at the Kennedy Institute of Rheumatology. He joined Imperial College in 1998 and has been based at the Chelsea & Westminster since 2001.
Supported by the Wellcome Trust, Medical Research Council, Biotechnology and Biological Sciences Research Council and other charity/industry grants, Professor Takata has established an internationally recognised unique translational research programme in the field of respiratory and critical care medicine at Imperial College. His research group (Critical Care Research Group) consists of a number of postdocs, research assistants and students, including both basic scientists and clinicians. The group investigates the molecular and inflammatory mechanisms of acute lung injury, ventilator-induced lung injury and sepsis-associated organ injury, using in vivo mouse models as the main paradigm with complementary in vitro cell biology, ex vivo isolated organ preparations and clinical studies.
Specific interests include the tumour necrosis factor signalling, novel roles of monocytes and their subsets, and the development of new anti-inflammatory therapies in these disease models. Over the years the group has developed a wide range of active collaborations across the College and its affiliated NHS Trusts as well as other institutions within UK. Recent focus of the group is placed particularly on clinical translational studies investigating the innate immune system functions in perioperative, critical care, trauma and burns patients.
Patel BV, Wilson MR, O’Dea KP, Takata M. TNF-induced death signaling triggers alveolar epithelial dysfunction in acute lung injury. J Immunol. 2013 in press.
Wilson MR, Patel BV, Takata M. Ventilation with ‘clinically-relevant’ high tidal volumes does not promote stretch-induced injury in the lungs of healthy mice. Crit Care Med. 2012 Oct;40(10):2850-7.
Patel BV, Wilson MR, Takata M. Resolution of acute lung injury and inflammation - a translational mouse model. Eur Respir J. 2012 May;39(5):1162-70.
Bertok S, Wilson MR, Morley PJ, de Wildt R, Bayliffe A, Takata M. Selective inhibition of intra-alveolar p55 TNF receptor attenuates ventilator-induced lung injury. Thorax. 2012 Mar;67(3):244-51.
Scott AJ, O'Dea KP, O'Callaghan D, Williams L, Dokpesi JO, Tatton L, Handy JM, Hogg PJ, Takata M. Reactive oxygen species and p38 mitogen-activated protein kinase mediate tumor necrosis factor alpha-converting enzyme (TACE/ADAM-17) activation in primary human monocytes. J Biol Chem 2011;286(41):35466-76.
Wilson MR, O’Dea KP, Zhang D, Shearman AD, Goddard ME, van RooijenN, Takata M. Role of lung-marginated monocytes in an in vivo mouse model of ventilator-induced lung injury. Am J Respir Crit Care Med 2009;179(10):914-922.
O’Dea KP, WilsonMR,Dokpesi JO, Wakabayashi K, Tatton L, van RooijenN, Takata M. Mobilization and margination of bone marrow Gr-1 high monocytes during sub-clinical endotoxemia predisposes the lungs towards acute injury. J Immunol 2009; 182:1155-1166.
Wilson MR, Goddard ME, O'Dea KP, Choudhury S, Takata M. Differential roles of p55 and p75 tumor necrosis factor receptors on stretch-induced pulmonary edema in mice. Am J Physiol Lung Cell Mol Physiol 2007;293:L60-68.
O'Dea KP, Young AJ, Yamamoto H, Robotham JL, Brennan FM, Takata M. Lung-marginated monocytes modulate pulmonary microvascular injury during early endotoxemia. Am J Respir Crit Care Med 2005;172:1119-1127.
Wilson MR, Choudhury S, Goddard ME, O'Dea KP, Nicholson AG, Takata M. High tidal volume upregulates intrapulmonary cytokines in an in vivo mouse model of ventilator-induced lung injury. J Appl Physiol 2003;95:1385-1393.
et al., 2021, Secreted extracellular cyclophilin a is a novel mediator of ventilator induced lung injury., American Journal of Respiratory and Critical Care Medicine, ISSN:1073-449X
et al., 2021, Intra-alveolar neutrophil-derived microvesicles are associated with disease severity in COPD, American Journal of Physiology: Lung Cellular and Molecular Physiology, Vol:320, ISSN:1040-0605, Pages:L73-L83
et al., 2020, Intra-alveolar neutrophil-derived microvesicles predict development of primary graft dysfunction after lung transplantation, EUROPEAN RESPIRATORY SOC JOURNALS LTD, ISSN:0903-1936
et al., 2020, Late Breaking Abstract - Myeloid-derived microvesicles as acute mediators of sepsis-induced lung vascular inflammation, EUROPEAN RESPIRATORY SOC JOURNALS LTD, ISSN:0903-1936
Koh M, Takata M, Wilson M, 2020, Cyclophilin A as a Novel Mediator in Ventilator-Induced Lung Injury, Annual Meeting on Experimental Biology, WILEY, ISSN:0892-6638