Inflammation, Skin & Joint Diseases
Inflammation represents the coordinated immune response to infection, trauma and injury. When appropriately controlled, inflammation ensures competent host defence and prevents excessive damage of the affected tissue or organ structure. In chronic inflammatory diseases, this process is disrupted and instead of offering protection, drives disease progression.
Clinical Lead
Research Lead
Principal Investigators
Members of the inflammation, skin and joint disease theme research the molecular, cellular and immunological processes that drive host defence and chronic disease progression. These include studies into the mechanisms underlining chronic inflammatory conditions, cardiovascular disease, disorders in haemostasis and control of the inflammatory response to infection.
The group is built around a close interaction between basic and clinical researchers, and spans both novel discovery biology and translational studies. Internationally recognized research into the regulation of complement, cytokine and lipid signalling, coagulation, and various aspects of immune cell regulation and homeostatic turnover are central themes within the group. These activities are leading to novel prognostic, diagnostic and therapeutic approaches for direct patient benefit.
Selected Recent Publications
- Characterization of platelet aminophospholipid externalization reveals fatty acids as molecular determinants that regulate coagulation.
Clark SR, Thomas CP, Hammond VJ, Aldrovandi M, Wilkinson GW, Hart KW, Murphy RC, Collins PW, O'Donnell VB, Proc Natl Acad Sci U S A, Volume 110, 15 (April 2013) pp.5875-5880 - Steric analysis of epoxyalcohol and trihydroxy derivatives of 9-hydroperoxy-linoleic acid from hematin and enzymatic synthesis.
Thomas CP, Boeglin WE, Garcia-Diaz Y, O'Donnell VB, Brash AR, Chem Phys Lipids, Volume 167-168 (February 2013) pp.21-32 - Novel keto-phospholipids are generated by monocytes and macrophages, detected in cystic fibrosis, and activate peroxisome proliferator-activated receptor-γ.
Hammond VJ, Morgan AH, Lauder S, Thomas CP, Brown S, Freeman BA, Lloyd CM, Davies J, Bush A, Levonen AL, Kansanen E, Villacorta L, Chen YE, Porter N, Garcia-Diaz YM, Schopfer FJ, O'Donnell VB, J Biol Chem, Volume 287, 50 (December 2012) pp.41651-41666 - Sensitive and specific assays for C3 nephritic factors clarify mechanisms underlying complement dysregulation.
Paixão-Cavalcante D, López-Trascasa M, Skattum L, Giclas PC, Goodship TH, de Córdoba SR, Truedsson L, Morgan BP, Harris CL, Kidney Int, Volume 82, 10 (November 2012) pp.1084-1092 - Contractile, but not endothelial, dysfunction in early inflammatory arthritis: a possible role for matrix metalloproteinase-9.
Reynolds SL, Williams AS, Williams H, Smale S, Stephenson HJ, Amos N, George SJ, O'Donnell VB, Lang D, Br J Pharmacol, Volume 167, 3 (October 2012) pp.505-514