Imperial College London

Dr Kevin Woollard

Faculty of MedicineDepartment of Medicine

Senior Research Fellow
 
 
 
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Contact

 

+44 (0)20 3313 2357k.woollard Website

 
 
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Location

 

5N1BCommonwealth BuildingHammersmith Campus

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Summary

 

Summary

Dr Kevin Woollard received his PhD in 2003 and went on to perform postdoctoral studies at Baker IDI Heart & Diabetes Institute in Melbourne, Australia in collaboration with Roche (Basel, Switzerland) and fellowship funding from National Heart Foundation Australia.  In 2009 Dr Woollard returned to UK to work in the Divsion of Immunology & Inflammation at Kings College London through a British Heart Foundation Fellowship, studying monocyte heterogeneity in inflammatory diseases.  In 2012 Dr Woollard became a Non-Clinical Senior Lecturer in Medicine at Imperial College London.

My main interests are in the understanding of leukocyte biology in vascular inflammation.  How myeloid and other circulating blood cells contribute to inflammatory disease through mobilisation, recruitment and migration.  Utilising novel imaging modalities (e.g. intravital, MRI, FMT) to characterise the in-vivo effector functions at the endothelial interface and to understand the pathophysiology of chronic vascular inflammation, such as in atherosclerosis and autoimmune vasculopathies.

Selected key publications

Woollard KJ*, Kling D, Kulkarni S, Dart AM, Jackson S & Chin-Dusting J. (2006). Raised plasma soluble P-selectin in peripheral arterial occlusive disease enhances leukocyte adhesion. Circ. Res., 98; 149-156.  * Corresponding Author. Editorial Feature.

Kulkarni S, Woollard KJ*, Thomas S & Jackson S. (2007). Conversion of platelets from a pro-aggregatory to a pro-inflammatory adhesive phenotype: A role for PAF in the spatial regulation of neutrophil activation on thrombi. Blood.110:1879-1886.  * Joint 1st Author. Cover Feature.

Woollard KJ*, Suhartoyo A, Harris EE, Eisenhardt SU, Jackson SP, Peter K, Dart AM, Hickey MJ, Chin-Dusting JP. (2008) Pathophysiological levels of soluble P-selectin mediate adhesion of leukocytes to the endothelium through Mac-1 activation. Circ Res. 103: 1128-1238. * Corresponding Author.

Woollard KJ, Sturgeon S, Chin-Dusting JP, Salem HH, Jackson SP. (2009). Erythrocyte Hemolysis and Hemoglobin Oxidation Promote Ferric Chloride-induced Vascular Injury. J Biol Chem. 284: 13110-13118.

Murphy AJ, Woollard KJ. (2010). High density lipoprotein – A potent inhibitor of inflammation. Clin. Exp. Pharmacol. Physiol. 37: 710-718.

Cros J, Cagnard N, Woollard K*, Patey N, Zhang SY, Senechal B, Puel A, Biswas SK, Moshous D, Picard C, Jais JP, D'cruz D, Casanova JL, Trouillet C, Geissmann F. (2010). Human CD14dim Monocytes Patrol and Sense Nucleic Acids and Viruses via TLR7 and TLR8 Receptors. Immunity, 24: 375-386.  * Joint 1st Author. Editorial Feature.

Woollard KJ*, Geissmann F (2010). Monocytes in atherosclerosis: subsets and functions. Nat. Rev. Cardiol. 7: 77-86.  * Corresponding author.

Publications

Jackson WD, Weinrich TW, Woollard KJ, 2016, Very-low and low-density lipoproteins induce neutral lipid accumulation and impair migration in monocyte subsets, Scientific Reports, Vol:6, ISSN:2045-2322

Diaz AIG, Moyon B, Coan PM, et al., 2016, New Wistar Kyoto and spontaneously hypertensive rat transgenic models with ubiquitous expression of green fluorescent protein, Disease Models & Mechanisms, Vol:9, ISSN:1754-8403, Pages:463-471

Tarzi RM, Liu J, Schneiter S, et al., 2015, CD14 expression is increased on monocytes in patients with anti-neutrophil cytoplasm antibody (ANCA)-associated vasculitis and correlates with the expression of ANCA autoantigens, Clinical and Experimental Immunology, Vol:181, ISSN:0009-9104, Pages:65-75

Saja MF, Baudino L, Jackson WD, et al., 2015, Triglyceride-Rich Lipoproteins Modulate the Distribution and Extravasation of Ly6C/Gr1(low) Monocytes, Cell Reports, Vol:12, ISSN:2211-1247, Pages:1802-1815

Ling GS, Bennett J, Woollard KJ, et al., 2014, Integrin CD11b positively regulates TLR4-induced signalling pathways in dendritic cells but not in macrophages, Nature Communications, Vol:5, ISSN:2041-1723

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