Reader in Metabolism and Inflammation / British Heart Foundation Research Fellow
I graduated from the University of Naples “Federico II” (Italy) with a degree in Medical Biotechnology in 2002 and a PhD in Molecular Oncology and Endocrinology in 2007.
During my PhD (2002-07) I studied the pro-inflammatory and anti-apoptotic response controlled by the NF-kappaB family of transcription factors. In these studies I discovered novel mechanisms of activation of NF-kB downstream of TNF receptors and upon endoplasmic reticulum stress and the contribution of NF-kB activity to thyroid tumourigenesis (Biochem Biophys Res Comm 2003, J Biol Chem 2004, J Biol Chem 2006a, J Biol Chem 2006b, J Neurol Neurosurg Psychiatry 2008).
During my postdoc (2007-11) – supported in part by an Immediate Fellowship from the Italian Association for Cancer Research – I worked both at the University of Chicago (USA) and Imperial College (UK) at the identification of the molecular links between inflammation and metabolism in the adaptive immune system and in cancer (Proc Natl Acad Sci 2010, Nat Cell Biol 2011).
Since I moved to the William Harvey Research Institute in 2011, I focused on the investigation of the metabolic control of immune cell effector functions and the implications of the metabolic dependence of immune responses during inflammation. This work led to the award of a prestigious Intermediate Basic Science Research Fellowship from the British Heart Foundation in 2012 and the publication of a number of papers in the field (Mol Cell Proteomics 2014, PLoS Biol 2015, Trends Biochem Sci 2016, Eur J Immunol 2016, Cell Metab 2017, Nat Comm 2017).
Summary of Research
My focus is on the interconnections between metabolic and inflammatory pathways. We are investigating the hypothesis that systemic metabolic alterations in cardiovascular and autoimmune disease lead to aberrant immune cell responses and migration patterns, which favour the establishment of chronic inflammation. Our studies indicate that interfering with metabolic pathways (i.e., lipid, glucose and oxidative metabolism) alters immune cell effector functions (PLoS Biol 2015, Cell Metab 2017, Nat Comm 2017). In particular, we are focusing on the mechanisms of metabolic control of T cell-mediated immune responses, including migration, differentiation and cytokine production in physiology and under metabolic stress. These studies are providing insights into the role of energy balance on physiologic T cell-mediated immune responses and the effect of altering metabolism on the development of T cell-mediated inflammation, as well as new therapeutic targets to prevent inflammation in these human conditions.
Members of the Group
Dr Michelangelo Certo (British Heart Foundation-funded postdoctoral research assistant)
Dr Danilo Cucchi (British Heart Foundation-funded postdoctoral research assistant)
Dr Valentina Pucino (ARUK Clinical Research Fellow; co-supervised with Professor Pitzalis and Dr Bombardieri)
Mr David Tang (4th year medical student)
Dr Joanne Smith, Postdoc – Higher Scientific Officer at The Institute of Cancer Research London
Dr Robert Haas, PhD (2016) – Postdoc at The Francis Crick Institute
Dr Ken Cheung, PhD (2015) – Postdoc at QMUL
Ms Ridhika Poojara, MRes (2015) - Research assistant at Imperial College
Ms Claire Macdougall, MRes (2015) - PhD student at QMUL
Ms Jayna Narendra, MRes (2014) - PhD student at QMUL
Mr Shoaib Ansar Nasim, BSc (2016) - Medical student at Imperial College
Mr Chris Palmer-Jones, BSc (2014) - Medical student at QMUL
For a full list of publist publications click here
* denotes corresponding author
Papathanassiu AE*, Ko J-H, Imprialou M, Bagnati M, Srivastava PK, Vu HA, Cucchi D, McAdoo SP, Ananieva E, Mauro C* and Behmoaras J*. BCAT1 controls metabolic reprogramming in activated human macrophages and is associated with inflammatory diseases. Nat Comm, in press
Mauro C*, Smith J, Cucchi D, Coe D, Fu H, Bonacina F, Bagaretti A, Cermenati G, Caruso D, Mitro N, Catapano AL, Ammirati E, Longhi MP, Okkenhaug K, Norata GD and Marelli-Berg FM* (2017). Obesity-induced metabolic stress leads to biased effector memory CD4+ T cell differentiation via PI3K p110delta-Akt-mediated signals. Cell Metab, 25:593-609 10.1016/j.cmet.2017.01.008
Commentary in: Chapman NM and Hongbo C (2017). Dietary fat inflames CD4+ T cell memory in obesity. Cell Metab, 25:490-2 10.1016/j.cmet.2017.02.012
Pucino V, Bombardieri M, Pitzalis C and Mauro C* (2016). Lactate at the crossroads of metabolism, inflammation and autoimmunity. Eur J Immunol, 47:14-21 10.1002/eji.201646477
Haas R, Cucchi D, Smith J, Pucino V, Macdougall CE and Mauro C* (2016). Intermediates of metabolism: from bystanders to signaling molecules. Trends Biochem Sci, 41:460-71 10.1016/j.tibs.2016.02.003
Haas R, Smith J, Rocher-Ros V, Nadkarni S, Montero-Melendez T, D’Acquisto F, Bland EJ, Bombardieri M, Pitzalis C, Perretti M, Marelli-Berg FM* and Mauro C* (2015). Lactate regulates metabolic and pro-inflammatory circuits in control of T-cell migration and effector functions. PLoS Biol, 13:e1002202 10.1371/journal.pbio.1002202