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J Dalli Lab
Helping the body switch inflammation off — and stay well
We investigate how the body brings inflammation to a safe end after infection or injury. Our aim is to uncover the natural signals that protect tissues, support repair and prevent inflammation from becoming chronic disease.
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Connect with the group and related resolution biology networks.
Inflammation protects us. Failure to resolve it can cause disease.
Inflammation is essential: it helps the body fight infection and repair damage. The problem arises when this response does not switch off at the right time. Persistent inflammation can damage tissues and contributes to conditions including arthritis, cardiovascular disease and severe infection.
Our research focuses on the body’s own “resolution” pathways — active processes that restore balance without compromising host defence.
The body’s own resolution signals
Specialised pro-resolving mediators (SPMs) are naturally occurring molecules made from essential fatty acids, including omega-3 fatty acids. Rather than simply blocking inflammation, SPMs help immune cells clear infection and damaged tissue, limit unnecessary inflammation, and promote repair.
We study how these signals are made, how they act on immune cells, and how their failure contributes to disease. This knowledge can point to safer, more precise ways to treat inflammatory conditions.
Our research
01
Bone marrow and immune-cell programming
We are discovering how the bone marrow prepares immune cells before they enter the bloodstream. Our recent research shows that SPMs made within the marrow help programme neutrophils and monocytes for balanced responses to infection and injury.
02
How the body resolves inflammation
We investigate the cellular and molecular signals that allow inflammation to end safely. This work reveals how immune cells clear microbes and damaged tissue while restoring healthy organs.
03
New medicines for inflammatory disease
We use these discoveries to identify resolution-based approaches for conditions such as arthritis, cardiovascular disease and inflammatory bowel disease — aiming to restore protective immune balance rather than simply suppress inflammation.
04
Biomarkers and personalised treatment
We measure lipid mediators and immune-cell responses in patient samples to understand why disease develops, predict treatment response and help guide more personalised care.
New insights from the bone marrow
The bone marrow does more than make blood cells. It is also a place where immune cells learn how to respond.
In recent research, we found that developing red-blood-cell precursors, called erythroblasts, produce SPMs that help programme neutrophils — white blood cells that are vital for fighting infection. When this pathway was disrupted in experimental models, neutrophils became overactive, accumulated in tissues and were less effective at clearing infection. Restoring one SPM, RvD5n-3 DPA, helped re-establish balanced immune-cell function.
In complementary work, we showed that parasympathetic nerve signals support SPM production in bone marrow and help programme monocytes, another important immune-cell population. Loss of this pathway drove inflammatory monocyte and macrophage responses, while RvD5n-3 DPA restored key protective functions.
Together, these findings reveal a new way in which the body prepares immune cells for a measured, protective response — and identify resolution pathways as promising targets for inflammatory disease.
Bone marrow and immune-cell programming
The immune system is shaped before immune cells enter the circulation. We study how the bone-marrow environment programmes neutrophils, monocytes and macrophages so that they can fight infection effectively without causing excessive tissue damage.
Our recent work identifies erythroblasts as an important local source of SPMs. These signals help maintain normal neutrophil maturation and function. We have also found that parasympathetic signalling supports bone-marrow SPM production and influences how monocytes and their descendant macrophages respond during inflammation.
By defining these early programming steps, we aim to understand why immune responses become dysregulated in chronic inflammatory disease and identify opportunities to restore healthy immune function.
How the body resolves inflammation
Resolution is an active biological process. It involves switching off unnecessary inflammation while preserving the ability to control infection and repair damaged tissues.
We examine how SPMs and their receptors coordinate this process across immune cells and tissues. Our work addresses how these pathways control bacterial clearance, removal of dead cells, tissue repair and the return to homeostasis.
New medicines for inflammatory disease
Many current therapies control inflammation by suppressing parts of the immune system. We are investigating whether activating the body’s own resolution pathways can offer a complementary approach — one that limits harmful inflammation while supporting protective host defence and repair.
We develop and test new resolution-based therapeutic strategies across inflammatory and cardiovascular diseases, with a focus on rigorous target validation and clinically relevant models.
Biomarkers and personalised treatment
People with the same diagnosis can have very different immune profiles and responses to treatment. We use lipid-mediator profiling and immune-cell analysis to identify the molecular patterns associated with disease activity, recovery and therapeutic response.
Our goal is to develop biomarkers that support earlier diagnosis, better disease monitoring and more personalised treatment strategies.
Working towards healthier resolution
We combine molecular pharmacology, mass spectrometry, advanced immune-cell models and clinical research to understand how inflammation is resolved and translate these findings towards patient benefit.
Prof Jesmond Dalli
Lipid Mediator Unit,
Centre for Biochemical Pharmacology
John Vane Science Centre,
Charterhouse Square,
London, EC1M 6BQ, United Kingdom
Phone: +44 (0) 207 882 8263
Email: j.dalli@qmul.ac.uk
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