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Andrew Foey![]() Dr Andrew Foey
Role Qualifications & background
2006 PG Cert. Learning & Teaching in Higher Education University of Plymouth 1986 HND Applied Biology Bristol Polytechnic (now University of West of England)
Expertise
Cytokine Immunopathology in inflammatory conditions, monocyte /macrophage biology, cell-to-cell interactions, cell signalling, apoptosis and cell cytometry.
Previous appointments
MRC Career Development Fellowship in Nutritional Immunology, MRC Human Nutrition Research Unit, Cambridge, UK. May 2004 – July 2005. Senior Research Fellow, Kennedy Institute of Rheumatology, Imperial College, London, UK. July 1996 – December 2003. Post Doctoral Research Scientist, Bath Institute for Rheumatic Diseases, Bath, UK. October 1995 – June 1996. Research Assistant and SERC CASE PhD Studentship, Bath Institute for Rheumatic Diseases, Bath, UK. January 1992 – September 1995. Research Scientist Industrial Placement, Boots Pharmaceuticals, Nottingham, UK. July 1994 – December 1994. Research Assistant, MRC Tuberculosis and Related Infections Unit, RPMS Hammersmith Hospital, London, UK. September 1989 – December 1991. Research Assistant, Nuffield Department of Surgery, John Radcliffe Hospital, Oxford, UK. June 1991 – December 1991. Research Assistant, CDE Porton Down, Salisbury, UK. July 1987 – September 1988.
Research interests Macrophages are fundamental cells to innate immune mechanisms. They exist in two main subsets which are determined by the tissue environment; where both differentiation and activation signals play a role in determining subset effector functionality. M1-like macrophages are pro-inflammatory and display anti-tumour effects whereas the M2-like macrophage subset is anti-inflammatory, regulatory and pro-tumoural. It is unclear whether these two subsets represent distinct canonical forms of macrophage subset or whether there is a sliding scale of effector function between these two extremes. If the latter scenario exists, it is likely that the macrophages display a level of plasticity, hence macrophage function can be manipulated/controlled. The regulation of macrophage function represents a realistic cell-based therapeutic regimen and would be of benefit in the treatment of many diseases where the immunopathological mechanisms are predominated by dysfunctional macrophages. The focus of this research has centred on the role of mucosal macrophages in driving homeostatic healthy immune function and immunopathological mechanisms upon disruption of mucosal tolerance. The disease states currently under investigation include oral pathologies (chronic periodontitis, oral squamous cell carcinoma) and gastro-intestinal tract pathologies (Crohn’s disease, ulcerative colitis). Harnessing of both microbial (commensal and pathological) and dietary effects will allow for the regulation of macrophage function and may ameliorate the symptoms of such pro-inflammatory and suppressive disease states. Current avenues of research endeavour include: 1) Immunomodulatory role of probiotics – centred around the modulation of pro-inflammatory and anti-inflammatory cytokine production by specific macrophage subsets and upon contact-mediated interaction with gut epithelial cells. 2) Mechanisms of endotoxin tolerance mediated by oral pathogens and the relative subset sensitivities to tolerance-induction. 3) Application of oral pathogens and their PAMPs in immune-deviation in pro-inflammatory and suppressive immunopathologies. 4) Negative regulation and manipulation of macrophage plasticity in Crohn’s disease. 5) Immune cell cross-talk mechanisms involved in perpetuation of mucosal pathologies. 6) Role of oligosaccharides/b-glucans as modulators of macrophage-mediated immunity. 7) Dietary microparticles: immune activators or tolerance inducers? Publications
Habil, N., Abate Woldie, W., Beal, J. and Foey, A.D. (2012): Probiotic bacterial species selectively modulate gut epithelial cell beta-defensin-2. (Manuscript in preparation). Zhang, Z., Panesar, M., Isomaki, P., Foey, A., Owen, S., Douglas, J., McClinton, C., Russell, A., Vyse, T., Dazzi, F., Brennan, F. and Cope, A.P. (2007): Sustained downregulation of TCRz defines a transition from antigen mode to inflammation mode during T cell differentiation. Blood 109:4328-4335. Brennan, F.M., Foey, A.D. and Feldmann, M. (2006): The importance of T cell interactions with macrophages in rheumatoid cytokine production. Current Concepts in Autoimmunity and Chronic Inflammation, Current Topics in Microbiology and Immunology CTMI 305: 177-194. Invited review chapter. Foey, A.D., Foxwell, B.M.J. and Brennan, F.M. (2004): Conventional PKC and cAMP-dependent atypical PKCzeta differentially regulate macrophage production of TNFa and IL-10. Immunology 112:44-53.
Ozegbe, P., Foey, A.D., Ahmed, S. and Williams, R.O. (2004): Impact of cAMP on the T cell response to type II collagen. Immunology 111:35-40. Foey, A.D., Field, S., Ahmed, S., Jain, A., Feldmann, M., Brennan, F.M. and Williams, R.O. (2003): Impact of VIP and cAMP on the regulation of TNFa and IL-10 production: implications for rheumatoid arthritis. Arthritis Research and Therapy 5:R317-R328. Brennan, F.M. and Foey, A.D. (2002): Cytokine regulation in RA synovial tissue: role of T cell: macrophage contact dependent interactions. Arthritis Research 4:S177-S182. Invited review chapter. Foey, A.D., Green, P., Foxwell, B.M.J., Feldmann, M. and Brennan, F.M. (2002): Cytokine-stimulated T cells induce macrophage IL-10 production dependent on phosphatidylinositol 3-kinase and p70S6K: implications for rheumatoid arthritis. Arthritis Research 4: 64-70. Foey, A.D., Feldmann, M. and Brennan, F.M. (2001): CD40 ligation induces macrophage IL-10 and TNFa production: Differential use of the PI3K and p42/44 MAPK-pathways. Cytokine 16: 131-142. Foey, A.D., Feldmann, M. and Brennan, F.M. (2000): Route of monocyte differentiation determines their cytokine production profile: CD40 ligation induces interleukin-10 expression. Cytokine 12: 1496-1505. Foey, A.D., Parry, S.L., Williams, L.M., Feldmann, M., Foxwell, B.M.J. and Brennan, F.M. (1998): Regulation of monocyte IL-10 synthesis by endogenous IL-1 and TNF-a: Role of the p38 and p42/44 mitogen-activated protein kinases. J. Immunol. 160: 920-928. Foey, A.D., Crawford, A. and Hall, N.D. (1997): Modulation of cytokine production by human mononuclear cells following impairment of Na,K-ATPase activity. Biochem. Biophys. Acta. Mol. Cell Res. 1355: 43-49. Maubach, K., Foey, A.D. and Hall, N.D. (1993): Impaired activity of thiol-dependent ATPases in rheumatoid mononuclear cell membranes. Agents and Actions 39: C107-C109.
Published Abstracts
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