Hawkins Group - Redox Biology

Our focus is to gain a better understanding of the role of innate immune cell dysfunction in the development of chronic inflammatory disease, particularly atherosclerosis and the development of cardiovascular complications in diabetes.





Our research is focused on understanding how neutrophil-derived products alter cellular function and promote tissue damage and the development of chronic inflammatory disease. We are particularly interested in the role of extracellular traps and their components, and reactive oxidants produced by myeloperoxidase. One of our key aims is to gain new insight into how oxidation during inflammation drives vascular and immune cell dysfunction. This is important for the development of new therapeutic approaches to decrease tissue damage sustained during chronic inflammation, particularly in diseases like atherosclerosis.



  • In vitro immune and vascular cell models (cells lines, primary cells).
  • Visualisation and quantification of extracellular traps.
  • Biochemical and cellular assays, molecular biology techniques and assessment of reactive intermediates and markers of oxidative stress.
  • Analytical methodology, including high performance liquid chromatography (HPLC; for various analytes, oxidation products) and electron paramagnetic resonance spectroscopy (EPR, for free radicals, metal ions).









Chronic inflammation is a repetitive cycle of immune cell infiltration and activation that underlies the development of many diseases. Activated immune cells release the enzyme myeloperoxidase, which catalyses the reaction of hydrogen peroxide with chloride ions to form the potent oxidant hypochlorous acid (HOCl) - the active component in bleach. This oxidant rapidly kills microbes to combat and prevent the spread of infection. However, excessive production of HOCl in chronic inflammation causes extensive, irreversible host tissue damage, which results in disease.

Immune cells also release extracellular traps, as an additional way to help immobilise and kill pathogens. These traps consist of a mesh of DNA and histones and contain many other proteins, including those with an anti-microbial function such as myeloperoxidase. Although these traps are a key innate immune defense, they are also known to promote inflammation and thrombosis. This also damages the host and ultimately leads to life-threatening vascular complications and organ damage.

Our group is working to gain a more detailed understanding of how oxidants and extracellular traps contribute to the development of disease to allow us to design new strategies to therapeutically target these reactions. Our aim is to develop a treatment to limit damaging reactions to the host during chronic inflammation without compromising innate immune defences.



Our current research projects are listed below. We are always looking for motivated Bachelors’ and Masters’ students to join the Redox Biology Group and work on these ongoing projects. 

  • Understanding the protective mechanisms of selenocyanate in chronic inflammatory disease.
  • Examining the role of post-translational histone modification in inflammation.
  • Understanding the role of macrophage extracellular traps in disease.
  • Investigating the role of nucleic acid modification in diabetes and inflammatory disease.

Understanding the protective mechanisms of selenocyanate in chronic inflammatory disease

This project examines a new approach to reduce tissue damage during chronic inflammatory diseases like atherosclerosis without compromising innate immunity. 

Immune cells produce hypochlorous acid (HOCl) to kill bacteria. However, the over-production of HOCl during chronic inflammation causes host cell damage and disease, including atherosclerosis. There are a lack of effective treatments to prevent tissue damage by HOCl during chronic inflammation without affecting pathogen killing. In this project, we will examine whether selenocyanate (SeCN) can prevent tissue damage on exposure to HOCl without affecting innate immunity. Our pilot data show that SeCN readily scavenges HOCl and decreases vascular cell damage. This produces hyposelenocyanous acid (HOSeCN), which kills bacteria but is less toxic to host cells. We will identify the pathways by which SeCN prevents HOCl-induced cell damage and characterise the reactivity of HOSeCN with cells to assess the potential for this approach to be used to modulate inflammatory disease in vivo. Overall, this work could improve the treatment of atherosclerosis and a wide-range of other inflammatory disorders. 

Examining the role of post-translational histone modification in inflammation

This project examines the dark side of histones, the nuclear proteins that package DNA but can promote organ failure and death when outside the cell. 

Histones are proteins usually found in the nucleus of the cell, which stabilise DNA and regulate cell function. However, injury to cells and the release of extracellular traps by immune cells results in the presence of histones outside cells. This can be beneficial, as histones kill bacteria and can limit the spread of infection. However, histone toxicity is not specific to pathogens and these proteins also damage host tissue, which can lead to organ failure and death. Post translational modification is critical in controlling histone function inside the cell. However, it is not clear how modifications to histones affect their reactions when they are outside the cell. In this project, we will characterise the modifications found on extracellular histones released during chronic inflammation, and then examine how these modifications influence the reactivity of histones with human cells. This will provide valuable insight into disease mechanisms needed for the design of new drug treatments.

Understanding the role of macrophage extracellular traps in disease

This project examines a potential new pathway by which macrophages promote lipid accumulation and lesion development in atherosclerosis.

Human THP-1 macrophages treated with TNFa to release extracellular traps. Image shows DNA released from the cells stained with SYTOX green.

Macrophages infiltrate the artery wall in atherosclerosis, where they accumulate lipid and drive the formation of lesions. Macrophages also release extracellular traps under the inflammatory conditions seen in atherosclerosis. Extracellular traps consist of a mesh of DNA and histones, with the traps released by neutrophils known to be strongly linked with the development of disease. It is not well established whether macrophage traps also have a pathological role, though these structures are present in human atherosclerotic tissue. The focus of this project therefore is to examine the pathways by which macrophage traps contribute to lesion development in atherosclerosis by identifying their role in driving inflammation, lipoprotein modification and vascular dysfunction. This is important for the development of novel approaches to prevent extracellular trap release, as a therapeutic strategy to mitigate atherosclerosis, one of the biggest killers in Europe.

Investigating the role of nucleic acid modification in diabetes and inflammatory disease

This project examines how the oxidative modification of RNA and DNA perturbs cellular function to promote inflammation, pancreatic islet dysfunction and vascular damage.

The chemistry of hypochlorous acid (HOCl) in biological systems has attracted considerable attention, as excessive or misplaced production of this chemical during prolonged inflammation, where there is an infiltration of leukocytes, damages host tissue, which contributes to the development of disease. HOCl modifies the nucleoside building blocks of RNA and DNA, resulting in the formation of both oxidised and chlorinated products, which are present in inflammatory fluids and diseased tissue. Currently, whether these modified nucleosides play a role in disease pathology is not well understood. This is particularly significant given the presence of DNA within extracellular traps, and its close proximity to myeloperoxidase. In this project, we will examine how the modification of nucleic acids contributes to the development of oxidative stress and inflammation in different cell types, particularly pancreatic b-cells, as RNA oxidation is strongly associated with diabetic mortality, but the mechanisms responsible are not known.









  • Independent Research Fund Denmark (Danmarks Frie Forskningsfond), Project Grant, Understanding the protective mechanisms of selenocyanate in inflammatory disease (2022).
  • Royal Society of Chemistry (UK) Development Grant, Modulation of immune cell extracellular trap formation during inflammation (2021).
  • Novo Nordisk Foundation (Denmark) Biomedical Project Grant, Characterisation of immune cell extracellular traps and their role in driving inflammation and atherosclerosis (2019).
clare hawkins

Group Leader

 Clare Hawkins
 Professor MSO

 Phone +45 3533 7005

 ORCID: 0000-0003-2738-5089

Group members

Name Title Phone E-mail
Els Alletta Hartsema PhD Fellow   E-mail
Josje Maria Aline Huisman Master Student   E-mail
Sussi Mørkeberg Kristoffersen Laboratory Technician +4524637153 E-mail