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Department of Pharmacology



bulmerDr David Bulmer - Group leader

University Assistant Professor

E-Mail: dcb53 [at]
Tel: +44 (0) 3 34047



Visceral, pain, nociception, translational, irritable bowel syndrome, inflammatory bowel disease


Investigator biography

David Bulmer studied pharmacology at the University of Manchester, and obtained his PhD in physiology (central processing of sensory input from the heart) with Prof Mike Spyer at University College London. Following post-doctoral training with Prof David Grundy on sensory function in the gastrointestinal tract at the University of Sheffield, David joined the Neuroscience & Gastrointestinal Centre of Excellence in Drug Discovery (CEDD) at GlaxoSmithKline as an electrophysiologist in the visceral pain group, progressing to lead a translational research group within the Immuno-Inflammation CEDD. David left GSK in 2009, joining Queen Mary University of London (QMUL) on a Medical Research Council funded Skills Gap Award as a lecturer in Neurogastroenterology. At QMUL, David established a word class translational neuroscience group based on the use of human tissue to study the mechanisms of sensory signalling from gut in health and disease. A notable achievement of his group have been the development of “first in man” recordings and subsequent detailed characterisation of human visceral nociceptors. In July 2017, David joined the Department of Pharmacology, University of Cambridge, where he has quickly established a translational human tissue lab.  

Research summary

Abdominal pain is a leading cause of morbidity in gastrointestinal disease. Despite this we still know little of how pain is triggered in “functional” gastrointestinal disorders such as irritable bowel syndrome (IBS), in which no overt clinical pathology can be detected. Furthermore, in organic diseases such as inflammatory bowel disease (IBD), previous assumptions that treating the inflammation would resolve the pain appear to be only partly true, with a significant proportion of patients reporting pain while in clinical remission.

One hypothesis supported by work from my lab and others, is that the bowel of IBS or IBD patients produces pro-nociceptive mediators capable of stimulating pain sensing nerves (nociceptors), which relay signals (nociception) to the brain where it is interpreted as pain. This process is referred to as peripheral sensitisation, and we believe it is an important cause of pain in patients with IBS and IBD. Using human tissue based approaches we have been able to identify a critical role for the voltage gated sodium channel subtype NaV1.9 in the activation of visceral nociceptors by pro-nociceptive mediators released from the bowel of IBS and IBD patients, and discovered a previously unrecognised role of Matrix Metalloproteinases in the activation of visceral nociceptors in IBD. Work now continues to further understand the mediators and mechanisms of peripheral sensitisation in gastrointestinal disease with an ultimate goal of developing effective visceral analgesics for the treatment of pain in IBS and IBD.


Key publications


  • Bautzova T, Hockley JRF, Perez-Berezo T, Pujo J, Tranter MM, Desormeaux C, Barbaro MR, Basso L, Le Faouder P, Rolland C, Malapert P, Moqrich A, Eutamene H, Denadai-Souza A, Vergnolle N, Smith ESJ, Hughes DI, Barbara G, Dietrich G, Bulmer DC, Cenac N. (2018) 5-oxoETE triggers nociception in constipation-predominant irritable bowel syndrome through MAS-related G protein-coupled receptor D. Sci Signal. 11(561). epub

  • McGuire C, Boundouki G, Hockley JRF, Reed D, Cibert-Goton V, Peiris M, Kung V, Broad J, Aziz Q, Chan C, Ahmed S, Thaha MA, Sanger GJ, Blackshaw LA, Knowles CH, Bulmer DC. (2018) Ex vivo study of human visceral nociceptors. Gut. 67(1):86-96. 

  • Hockley JR, Boundouki G, Cibert-Goton V, McGuire C, Yip PK, Chan C, Tranter M, Wood JN, Nassar MA, Blackshaw LA, Aziz Q, Michael GJ, Baker MD, Winchester WJ, Knowles CH, Bulmer DC. (2014) Multiple roles for NaV1.9 in the activation of visceral afferents by noxious inflammatory, mechanical, and human disease-derived stimuli. Pain. 155(10):1962-75.