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Steve Edwards PhD

Steve Edwards, PhD

Edwards Group

University of Liverpool
Institute of Integrative Biology
Biosciences Building
Crown Street
L69  7ZB

Tel: 0151 7954553
Fax: 0151 7954414
Twitter: @SWE_lab


Our group is based within the Institute of Integrative Biology at the University of Liverpool.  Our key research areas are: the regulation of neutrophil functions, apoptosis and gene expression during inflammation and in inflammatory diseases; the role of the immune system in Complex Regional Pain Syndrome; and the regulation of apoptosis in cancer.

Neutrophil Function in Inflammatory Disease
There is a growing appreciation of the role of the neutrophil in diseases such as rheumatoid arthritis (RA), where activated neutrophils can contribute to damage to host tissue.  We are carrying-out whole transcriptome analysis of RA neutrophils, alongside healthy neutrophils treated in vitro with mediators of inflammation (cytokines, immune complexes etc).  This will build a model of gene expression in inflammatory neutrophils, and to try to understand why some RA patients respond well to therapy and why others do not.  One marker identified by transcriptomic analysis of RA neutrophils is Nampt.  We are currently characterizing the effects of Nampt, and its inhibitor (FK866), on neutrophil functions and expression profile.

Neutrophils and Juvenile Lupus (JSLE)
In juvenile systemic lupus erythematosus (JSLE), the process of neutrophil apoptosis occurs sooner than in neutrophils from healthy children, and we believe this is an important mechanism which contributes to low neutrophil counts (neutropenia) seen in JSLE, and perhaps autoantibody production.  We want to understand which factor(s) within the blood of children with JSLE are responsible for increased apoptosis, and how this is controlled at the cellular level.  We are also interested in finding out whether the normal function of neutrophils from JSLE children is impaired e.g. ability to phagocytose and kill bacteria.  

Complex Regional Pain Syndrome
Complex Regional Pain Syndrome (CRPS) is a long lasting pain condition which usually develops after a minor injury or fracture. The cause of the disease is unknown but research has shown that dysfunction of the immune system plays a role in the development and maintenance of CRPS.  We are researching how immune cells in the skin of patients with CRPS are different from those in healthy individuals, and how the nervous system interacts and directs immune cell responses.

Chronic Myeloid Leukaemia
Chronic Myeloid Leukaemia (CRPS) is caused by over-expression of the tyrosine kinase Bcr-Abl, leading to increased cell division and unregulated growth of bone marrow cells. There are several drug therapies (Imatinib, Dasatinib, Nilotinib and Bosutinib) available which can block the action of Bcr-Abl.  However, a proportion of patients do not respond to these drugs and resistance can develop.  Our research is investigating the cellular processes that lead to abnormal cell growth and apoptosis in CML, and the downstream consequence of tyrosine kinase inhibition. We are also interested in finding new ways to induce apoptosis in CML cells that are resistant to tyrosine kinase inhibition.  


Edwards GroupGroup Members (L-R)

Kate Roberts, BSc
Scott Osborne, MSc
Lynn Ellwood, MPhil
Steve Edwards, PhD
Helen Wright, PhD
Direkrit (Danny) Chiewchengchol, MD
Huw Thomas, MRes


Recent publications

Wright HL, Bucknall RC, Moots RJ and Edwards SW. (2011) Analysis of synovial fluid and plasma cytokines provides insights into the mechanisms of inflammatory arthritis and may predict response to therapy.
Rheumatology. Epub doi:10.1093/rheumatology/ker338.

Wright HL, Chikura B, Bucknall RC, Moots RJ, Edwards, SW (2011) Change in expression of membrane TNF, NFkappaB activation and neutrophil apoptosis during active and resolved inflammation.
Annals of the Rheumatic Diseases 70(3), 537-43

Barnes TC, Spiller D, Anderson ME, Edwards SW, Moots RJ. (2011) Endothelial cell activation and apoptosis mediated by neutrophil-dependent interleukin 6 trans-signalling: a novel target for systemic sclerosis?
Annals of the Rheumatic Diseases 70(2) 366-372

Midgley, A, Mayer, K, Edwards, SW and Beresford, MW. (2011) Differential expression of factors involved in the intrinsic and extrinsic apoptotic pathways in Juvenile Systemic Lupus Erythematosus. 
Lupus 20, 71-79  
Barnes TC, Cross A, Anderson ME, Edwards SW and Moots RJ. (2011) Relative alpha1-antitrypsin deficiency in systemic sclerosis.
Rheumatology 50(8), 1373-8  

Halfhide, CP, Flanagan, BF, Brearey, SP,  Hunt, JA,  Fonceca, AM, McNamara, PM, Howarth, D, *Edwards, SW and *Smyth, RL. (2011). Respiratory Syncytial Virus infects neutrophils in infants with severe bronchiolitis.
J. Infect. Dis 204, 451-458

Wright HL, Moots RJ, Bucknall RC, Edwards SW. (2010) Neutrophil function in inflammation and inflammatory diseases.
Rheumatology 49(9), 1618-31

Thomas, LW, Lam, C and Edwards, SW. (2010) Mcl-1: the molecular regulation of protein function.
FEBS Lett 584, 2981-2989

Midgley A, McLaren Z, Moots RJ, Edwards SW and Beresford MW. (2009) The role of neutrophil apoptosis in juvenile onset Systemic Lupus Erythematous.
Arthritis and Rheumatism 60, 2390-2401

Halfhide, CP, Brearey SP, Flanagan BF, Hunt JA, Howarth J, Cummerson J, Edwards, SW, Hart CA and Smyth RL.  (2009). Neutrophil TLR4 protein expression is reduced in the airways of infants with severe bronchiolitis.
Thorax 64, 798-805

Cross A, Moots R J and Edwards S W (2008) The dual effects of TNFa on neutrophil apoptosis are mediated via differential effects on expression of Mcl-1 and Bfl-1.
Blood 111(2), 878-84

Subramanian, S, Roberts, CL, Hart, CA, Martin, HM, Edwards, SW, Rhodes, JM and Campbell, BJ. (2008). Replication of colonic Crohn's Disease mucosal Escherichia coli isolates within macrophages and their susceptibility to antibiotics.
Antimicrobial Agents and Chemotherapy. 52, 427-434.

Pritchard, D.M., Berry, D., Przemeck, S. M. C. Campbell, F. Edwards, S. W. and Varro, A. (2008). Gastrin increases Mcl-1 expression in type I gastric carcinoid tumors and a gastric epithelial cell line that expresses the CCK-2 receptor.
Am J Physiol Gastrointest Liver Physiol. 295, G798 - G805