Dr Clett Erridge

Dr Clett Erridge

Honorary Research Fellow 

Tel: 0116 258 3365

Email: ce55@le.ac.uk

Address: Department of Cardiovascular Sciences, University of Leicester, Clinical Sciences Wing, Glenfield General Hospital, Leicester, LE3 9QP. 

Research interests

Atherosclerosis is a chronic inflammatory disease of the arteries that represents the root cause of the majority of heart attacks and strokes. Work in my laboratory aims to identify the primary agents responsible for promoting the inflammatory signals that underpin this disease, with a particular emphasis on investigation of the mechanisms connecting innate immune receptor signalling with the acute phase response and lipid metabolism.

PAMP image

Our recent work focuses on the mechanisms by which pathogen-associated molecular patterns (PAMPs, which are molecules expressed by microbes but not human cells that are detected by pattern-recognition receptors of the innate immune system), modify systemic inflammatory tone and regulate lipid metabolism at the cellular and systemic levels. Specific interests include: (i) the mechanisms by which innate immune receptor signalling regulates macrophage cholesterol and fatty acid uptake, synthesis and efflux in the context of foam cell formation, (ii) the regulation of innate immune function by factors associated with the Western diet, (iii) the contribution of commensal microbiota-derived PAMPs to the regulation of systemic inflammatory tone and (iv) the means of communication and lipid exchange between hepatocytes and macrophages during the acute phase response. We are currently investigating the contribution made by each of these pathways to atherosclerosis using a variety of models including in vitro cell culture and studies in human subjects.

Our aim is to use an improved understanding of these pathways to develop novel therapeutic approaches for the treatment or prevention of atherosclerosis and related metabolic diseases. We therefore have an active interest in the discovery and pre-clinical testing of novel anti-inflammatory and lipid regulatory lead molecules derived from high throughput screening of our natural product libraries for inhibitors or stimulants of specific pathways identified in our mechanistic studies (see Nutraceutical Discovery Resource pages).

Research Degree Supervision

I would be interested in supervising PhD study in the following areas:

  • Roles of innate immune signalling in macrophage lipid metabolism and atherosclerosis
  • Mechanisms of reverse cholesterol transport regulation during the acute phase response
  • Diet-dependent regulation of systemic inflammatory tone 

Key Publications

Herieka M, Faraj TA, Erridge C. Reduced dietary intake of pro-inflammatory Toll-like receptor stimulants favourably modifies markers of cardiometabolic risk in healthy men. Nutr Metab Cardiovasc Dis 2016 26:194-200

Nelson CP, Schunkert H, Samani NJ, Erridge C. Genetic analysis of leukocyte type-I interferon production and risk of coronary artery disease. Arterioscler Thromb Vasc Biol 2015 35:1456-62

Erridge C, Gracey J, Braund PS, Samani NJ. The 9p21 locus does not affect risk of coronary artery disease through induction of type 1 interferons. J Am Coll Cardiol 2013 62:1376-81

Erridge C. The capacity of foodstuffs to induce innate immune activation of human monocytes in vitro is dependent on food content of stimulants of Toll-like receptors 2 and 4. Br J Nutr 2010 Jan; 20 1-9

Erridge C. Endogenous ligands of TLR2 and TLR4: agonists or assistants? J Leukoc Biol. 2010 Jun; 87 6 989-99

Erridge C, Samani NJ. Saturated fatty acids do not directly stimulate Toll-like receptor signalingArterioscler Thromb Vasc Biol. 2009 Nov; 29 11 1944-9

Erridge C, Kennedy S, Spickett CM, Webb DJ. Oxidized phospholipid inhibition of toll-like receptor (TLR) signaling is restricted to TLR2 and TLR4: roles for CD14, LPS-binding protein, and MD2 as targets for specificity of inhibitionJ Biol Chem. 2008 Sep 5 283 36 24748-59

Erridge C. The roles of pathogen-associated molecular patterns in atherosclerosisTrends Cardiovasc Med. 2008 Feb 18 2 52-6

Erridge C, Attina T, Spickett CM, Webb DJ. A high-fat meal induces low-grade endotoxemia: evidence of a novel mechanism of postprandial inflammation. Am J Clin Nutr. 2007 Nov 86 5 1286-92

Erridge C, Spickett CM, Webb DJ. Non-enterobacterial endotoxins stimulate human coronary artery but not venous endothelial cell activation via Toll-like receptor 2Cardiovasc Res. 2007 Jan 1 73 1 181-9

Erridge C, Webb DJ, Spickett CM. Toll-like receptor 4 signalling is neither sufficient nor required for oxidised phospholipid mediated induction of interleukin-8 expressionAtherosclerosis. 2007 Jul 193 1 77-85

Erridge C, Stewart J, Poxton IR. Monocytes heterozygous for the Asp299Gly and Thr399Ile mutations in the Toll-like receptor 4 gene show no deficit in lipopolysaccharide signallingJ Exp Med. 2003 Jun 16 197 12 1787-91


Recent Papers

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