Professor Masao Takata

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 intensivist/anaesthetist in Japan and Canada. He started his research career in the field of cardiorespiratory systems physiology at Johns Hopkins in the USA, and on his return to Japan he moved to his current research area, i.e. mechanisms of acute lung injury.  After a sabbatical studying molecular biology at Harvard in the USA, he joined the Department of Anaesthetics at Imperial College in 1998.

 

Research Interests:

Supported by the Wellcome Trust, MRC, BBSRC and other charity/industry grants, Professor Takata has established a 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 employs a combined physiological and immunological approach, using in vivo murine models as the main paradigm with complementary in vitro cell biology, ex vivo isolated organ preparations and clinical studies.  Particular emphasis is placed on the understanding of the inflammatory mechanisms of the disease processes in perioperative and critical care to develop future therapeutic applications.

Currently the group’s major research focuses are:

1. Novel TNF-mediated mechanisms and therapies in acute lung injury and ventilator-induced lung injury
2. Roles of monocyte-endothelial interactions in lung injury and sepsis-associated organ injury
3. Clinical translational studies focusing on cytokine biology and innate immune system functions in perioperative, critical care and trauma patients

 

Key Publications:

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 2011 in press.

Patel BV, Wilson MR, Takata M.  Resolution of acute lung injury and inflammation – a translational mouse model. Eur Resp J 2011 in press.

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.

Dorr AD, Wilson MR, Wakabayashi K, Waite AC, Patel BV, van Rooijen N, O'Dea KP, Takata M.  Sources of alveolar soluble TNF receptors during acute lung injury of different etiologies. J Appl Physiol  2011;111(1):177-84.

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.