I established my research group at Imperial College London in 2010 within the Centre of Complement and Inflammation Research, Division of Immunology and inflammation.
The group received funding from the Medical Research Council, Wellcome Trust and Kidney Research UK. Our main interest in to understand genetic variation that controls macrophage function and to establish the link between genome-macrophage function-complex disorders. We use animal models (rats and mice) of inflammatory kidney disease, wound healing and fibrosis and apply systems-genetics approaches to investigate the effect of germline sequence variation on macrophage plasticity. In addition, our recent approaches pointed towards the importance of macrophage metabolism in inflammatory disease. http://www3.imperial.ac.uk/newsandeventspggrp/imperialcollege/newssummary/news_11-7-2017-12-50-54
Our main external collaborators are Dr Enrico Petretto at Duke-NUS, Singapore (https://www.duke-nus.edu.sg/content/petretto-enrico); Professor David Abraham at University College London (https://iris.ucl.ac.uk/iris/browse/profile?upi=DJABR26).
In addition, we work closely with the Molecular Endocrinology Group at Imperial College London (Profs Graham Williams and Duncan Bassett) as part of an OBCD collaborator (http://www.boneandcartilage.com/phenotyping.html).
SELECTED KEY PUBLICATIONS
2017 Papathanassiu AE, Ko JH, Imprialou M, Bagnati M, Srivastava PK, Vu HA, Cucchi D, McAdoo SP, Ananieva EA, Mauro C and Behmoaras J. BCAT1 controls metabolic reprogramming in activated human macrophages and is associated with inflammatory diseases. Nat Commun. 2017 Jul 12;8:16040.
2017 Chen TD, Rotival M, Chiu LY, Bagnati M, Ko JH, Srivastava PK, Petretto E, Pusey CD, Lai PC, Aitman TJ, Cook HT and Behmoaras J. Identification of Ceruloplasmin as a Gene that Affects Susceptibility to Glomerulonephritis Through Macrophage Function. Genetics. 2017 Jun;206(2):1139-1151.
2015 Rotival M, Ko JH, Srivastava PK, Kerloc'h A, Montoya A, Mauro C, Faull P, Cutillas PR, Petretto E and Behmoaras J. Integrating phosphoproteome and transcriptome reveals new determinants of macrophage multinucleation. Mol Cell Proteomics. 2015 Mar;14(3):484-98.
2014 Kang H, Kerloc’h A, Rotival M, Xu X, Zhang Q, D’Souza Z, Kim M, Scholz JC, Ko JH, Srivastava PK, Genzen JR, Cui W, Aitman TJ, Game L, Melvin JE, Hanidu A, Dimock J, Zheng J, Souza D, Behera AK, Nabozny G, Cook HT, Bassett JHD, Williams GR, Li, J, Vignery A, Petretto E and Behmoaras J. Kcnn4 is a regulator of macrophage multinucleation in bone homeostasis and inflammatory disease. Cell Reports, 2014 Aug 21;8(4):1210-24.
2013 Hull RP, Srivastava PK, D'Souza Z, Atanur SS, Mechta-Grigoriou F, Game L, Petretto E, Cook HT, Aitman TJ and Behmoaras J. Combined ChIP-Seq and transcriptome analysis identifies AP-1/JunD as a primary regulator of oxidative stress and IL-1β synthesis in macrophages. BMC Genomics. 2013 Feb 11;14:92.
2013 Deplano S, Cook HT, Russell R, Franchi L, Schneiter S, Bhangal G, Unwin RJ, Pusey CD, Tam FW and Behmoaras J. P2X7 receptor mediated Nlrp3 inflammasome activation is a genetic determinant of macrophage-dependent crescentic glomerulonephritis. J Leukoc Biol. 2013 Jan;93(1):127-34.
2012 Page TH, D'Souza Z, Nakanishi S, Serikawa T, Pusey CD, Aitman TJ, Cook HT, and Behmoaras J. Role of novel rat-specific Fc receptor in macrophage activation associated with crescentic glomerulonephritis. J Biol Chem. 2012 Feb 17;287(8):5710-9.
2011 Cook HT, Tarzi R, D’Souza Z, Gaelle L, Lin Wei-Chou, Aitman TJ, Mechta-Grogoriou F and Behmoaras J. AP-1 Transcription Factor JunD Confers Protection from Accelerated Nephrotoxic Nephritis and Control Podocyte-Specific Vegfa Expression. Am. J. Pathol. 2011 Jul;179(1):134-40.
2010 Behmoaras J, Smith J, D’Souza Z, Bhangal G, Chawanasuntoropoj R, Tam FW, Pusey CD, Aitman TJ, Cook HT. Multilocus protection from crescentic glomerulonephritis in the rat provides new insights into the genetics of macrophage activation. J Am Soc Nephrol. 2010 Jul;21(7):1136-44.
2008 Behmoaras J, Bhangal G, Smith J, McDonald K, Mutch B, Lai PC, Domin J, Game L, Salama A, Foxwell B, Pusey C, Cook T, Aitman T. JunD is a determinant of macrophage activation and is associated with susceptibility to glomerulonephritis. Nat Genet. 2008; 40:553-9.
et al., Changes in macrophage transcriptome associate with systemic sclerosis and mediate GSDMA contribution to disease risk, Annals of the Rheumatic Diseases, ISSN:0003-4967
et al., 2017, BCAT1 controls metabolic reprogramming in activated human macrophages and is associated with inflammatory diseases, Nature Communications, Vol:8, ISSN:2041-1723
et al., 2017, Identification of Ceruloplasmin as a Gene that Affects Susceptibility to Glomerulonephritis Through Macrophage Function, Genetics, Vol:206, ISSN:0016-6731, Pages:1139-1151
et al., 2017, A Bayesian Approach for Analysis of Whole-Genome Bisulfite Sequencing Data Identifies Disease-Associated Changes in DNA Methylation, Genetics, Vol:205, ISSN:0016-6731, Pages:1443-1458
et al., 2017, Genome-wide analysis of differential RNA editing in epilepsy, Genome Research, Vol:27, ISSN:1088-9051, Pages:440-450