Serendipity Grants

Grant category: Serendipity Grants

Year: 2026

Geography: Australia

Buruli ulcer is a severe skin infection caused by a bacterium called Mycobacterium ulcerans. Treatment requires weeks of antibiotics and sometimes surgery, leaving patients with disability and scarring. While developing a new diagnostic test, we discovered a virus called 40C-del that infects and kills the Buruli ulcer bacterium very efficiently. This exciting finding suggests that 40C-del might be developed into a new treatment. In this project, we will investigate exactly how 40C-del attacks and destroys the bacterium and test whether combining it with another virus (D29) improves effectiveness. We will also examine whether the bacterium can become resistant and whether the virus remains stable under conditions relevant to future medical use. By the end of the project, we will know whether 40C-del can become a future therapy for Buruli ulcer. This serendipitous discovery could ultimately lead to safer, more targeted treatments for people affected by this neglected tropical disease.

Grant category: Serendipity Grants

Year: 2026

Geography: Sweden

Wounds do not always heal in the same way in everyone. Men and women can differ in how their skin repairs itself, but most research has focused on the effects of sex hormones. Our recent work suggests that the difference may go deeper: some genes that change during wound healing are also expressed differently in male and female skin. This project will explore whether male and female wounds use different molecular programs to repair damaged tissue. We will study human skin wounds using advanced technologies that allow us to analyze thousands of individual cells and see where important genes are active in the tissue. We will also study skin samples from transgender donors receiving hormone treatment, which may help us separate the effects of hormones from more intrinsic biological differences. Finally, we will test selected genes in human skin cell and wound models. This work may reveal new mechanisms of wound healing and support more precise treatments for chronic, non-healing wounds.

Grant category: Serendipity Grants

Year: 2026

Geography: Sweden

Allergic diseases such as atopic dermatitis and asthma often start early in life and can flare repeatedly. They are also linked to health problems outside the skin and lungs, including increased risk of blood clotting and cardiovascular disease, but the reasons are poorly understood. This project asks whether long-lasting “memory” immune cells involved in allergy, called ILC2s, can send signals to the bone marrow and change how blood cells are produced. We will use established mouse models of allergic inflammation together with advanced cell analysis, gene expression studies and functional tests of blood-forming stem cells. We will also compare key findings with human samples. By revealing how allergic inflammation affects the bone marrow, the project may uncover new explanations for allergy-associated comorbidities and identify future strategies to prevent long-term complications of allergic disease.

Grant category: Serendipity Grants

Year: 2026

Geography: United Kingdom

The skin is an important sensory organ, with nerve endings extending into its outer layer (the epidermis), to detect heat, cold and harmful stimuli. In some skin diseases and during cancer treatments, these nerves are damaged and withdraw from the epidermis. Instead of causing numbness, this often leads to chronic, difficult-to-treat pain; in cancer patients, it can limit treatment. But why this happens is not fully understood. We are studying how immune cells in the skin interact with nerve endings. In our models, we see nerve loss similar to patients. Unexpectedly, when the nerves try to regrow, we have discovered that they follow the paths made by other types of nerves (sympathetic nerves) and end up in the wrong place, near hair follicles rather than in the epidermis. We think this misdirected growth causes nerves to behave as if they are detecting danger, triggering pain. By understanding this process, we aim to find ways to guide nerves correctly and reduce chronic pain.

Grant category: Serendipity Grants

Year: 2026

Geography: USA

While studying skin bacteria, we made a surprising discovery: simple, painless nail clippings contain readable human genetic messages (mRNA). Scientists previously believed these delicate messages were completely destroyed as nail cells harden and die. This unexpected finding could revolutionize how we diagnose subungual melanoma, a deadly skin cancer growing under the nail. Currently, diagnosing this cancer requires a painful surgical biopsy of the nail bed, risking permanent deformity. Our discovery suggests we might detect this cancer, and understand its deeper biology, just by analyzing a painless clipping. To investigate this, we will collect nail clippings from patients with harmless dark spots and those with confirmed nail cancer. Using advanced technology, we will read the surviving genetic messages to identify a “signature” of the cancer. We will also explore if these clippings reveal how the tumor interacts with the immune system, paving the way for pain-free diagnostics.

Grant category: Serendipity Grants

Year: 2026

Geography: USA

We aim to understand how skin inflammation is suppressed by a surprising site: the nose. This proposal is motivated by two unexpected discoveries during our prior Leo-funded work. First, we found that some bacteria generate large immune responses when they colonize the nose peacefully, even when there is no evidence of infection. Second, we found that these nasal bacteria suppress the immune response in the skin, even though the skin is 100x larger than the nose. Therefore, we hypothesize that the nose is an overlooked site of immune regulation for the skin. We now aim to understand the molecular details of this nose-skin immune suppression. We also plan to study how nose-skin immune suppression changes our risk of eczema, psoriasis, infection, and cancer. Overall, we hope to understand how the bacteria that naturally colonize our nose regulate skin health and use these insights to develop new therapies for skin inflammation.

Grant category: Serendipity Grants

Year: 2025

Geography: Denmark

Thomas Sicheritz-Pontén serendipitously found that ~15% of sequenced phages encode two adjacent, independently active endolysin genes, often with distinct catalytic and binding domains. In one example, each enzyme is active on its own, and modelling suggests they also form a complex. While developing a custom endolysin predictor incorporating gene neighbourhood context, he detected genomic patterns missed by other tools. Most studies focus on individual lysins or domains, overlooking adjacent full-length endolysin genes. His large-scale analysis of 21k phage genomes revealed this hidden trend and a possible unrecognised lysis strategy hiding in plain sight.

The project will begin with phage AA002, which infects Staphylococcus hominis, a contributor to human body odour. Thomas Sicheritz-Pontén will clone, express, and purify its two endolysins, assess their activity alone and in combination, and investigate synergy and complex formation. Structural modelling will provide mechanistic insight. In parallel, he will mine publicly available phage genomes to identify additional dual-endolysin systems and prioritise further candidates for testing on skin-associated bacteria under skin-like conditions.

This study will define a novel category of cooperative phage lytic enzymes, offering insights into phage genome organisation and enzyme evolution. Beyond fundamental discovery, these enzymes could serve as precise, microbiome-friendly actives for non-antibiotic applications such as next-generation deodorants.

Grant category: Serendipity Grants

Year: 2025

Geography: United Kingdom

Skin fibrosis is often a sequela of suboptimal wound healing following significant epidermal and/or dermal injury (burns, trauma, major surgeries). Fibrotic material replaces native skin with dense, non-functional connective tissue, ultimately resulting in loss of function and – in the most severe cases – leading to debilitating skin pathologies that limit movement and prevent patient reintegration into society. Ferreira’s lab hosts the only colony of spiny mouse in the UK (Acomys cahirinus). The spiny is, to date, the only mammal capable of completely regenerating skin wounds with minimal scarring following self-amputation. Sofia Ferreira Gonzalez is currently exploring the contribution of different dermal populations to this fibrosis-free wound healing.

Unexpectedly, Sofia Ferreira Gonzalez and colleagues found that spiny dermal fibroblasts have a highly plastic phenotype and are able to convert to many other cell types (neurons, myocytes, chondrocytes). Moreover, they found that spiny fibroblasts secrete factors that enhance migration and proliferation of human dermal fibroblasts and protect them from cellular senescence. Sofia Ferreira Gonzalez aims now to explore these results, defining which mechanisms drive plasticity, migration and proliferation in spiny fibroblasts and adapting them to human fibroblasts. By doing so, Sofia Ferreira Gonzalez aims to establish a radically new approach to skin trauma focused on stimulating tissue regeneration rather than suppressing fibrosis, which has the potential to revolutionize both care and patient outcomes.

Grant category: Serendipity Grants

Year: 2025

Geography: USA

Organisms are continuously bathed in a rich milieu of olfactory compounds. Defined by their ability to elicit the sense of smell, these molecules, and the receptors that sense them, have profound biological importance. Humans have hundreds of olfactory receptors, but paradoxically these are often expressed outside of the nasal cavity and on immune cells. Their function in these contexts is almost entirely unknown. The serendipitous finding illustrates that: a) olfactory receptors are enriched in inflamed skin and on lesion infiltrating lymphocytes; and b) odorants directly modulate lymphocyte function. Understanding the role and molecular mechanisms of these pathways in inflammation may open new avenues for treating skin disease with promise for targeted topical approaches.

To explore this serendipitous finding, the research project will combine in vivo models of skin inflammation with expertise in multiomic analyses of hidradenitis suppurativa (HS) and pyoderma gangrenosum (PG) patient tissues. The study will determine if exposure to olfactory molecules modulates skin inflammation in vivo, functionally dissect immune cell intrinsic olfactory signaling, and identify signatures of pathway activity in HS and PG.

This work will provide insight into the fundamental biology of immune-olfactory signaling and determine if there is functional relevance for skin inflammation. The project will also test the implications for HS and PG, where novel therapeutic approaches are urgently needed.

Grant category: Serendipity Grants

Year: 2025

Geography: Denmark

“Stretch-mediated tissue expansion” is used to grow extra skin during breast reconstruction. A mouse model mimicking this clinical process was used to unravel fibroblast-epithelial crosstalk supporting keratinocyte self-renewal. Unexpectedly, the research project found that stretching alters gene expression in Schwann cells, which support nerve function, and reduces touch sensitivity. However, how stretching impacts skin nerves and sensation remains unclear. In light of this serendipitous discovery, the project now plans to investigate how Schwann cells contribute to the regeneration and re-innervation of peripheral sensory neurons in stretched skin.

The new research project – SkinSense – will explore how stretching affects peripheral sensory neurons and Schwann cells, which are key to skin sensation. Single-cell transcriptomics and high-resolution imaging will be used to study how peripheral sensory neurons are affected in terms of structure, function, and repair. Based on these findings, gene therapy approaches using adeno-associated viruses will be tested to restore nerve function and recover skin sensation.

Loss of skin sensitivity after breast reconstruction can greatly affect the quality of life of women. Yet, the reasons behind this sensory loss are not well understood. SkinSense aims to uncover the biological causes of this dysfunction and test ways to restore sensation. This research could lead to new treatments that improve sensory outcomes for patients undergoing reconstructive surgery.