Explore our grantees and awardees

Grant category: LEO Foundation Awards

Year: 2025

Geography: Germany

Grant category: LEO Foundation Dr Abildgaard Fellowships

Year: 2025

Geography: Denmark

Grant category: Education and Awareness Grants

Year: 2025

Geography: Denmark

Grant category: Education and Awareness Grants

Year: 2025

Geography: Denmark

Grant category: Education and Awareness Grants

Year: 2025

Geography: Denmark

Grant category: Serendipity Grants

Year: 2025

Geography: Denmark

Vision: We 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, we detected genomic patterns missed by other tools. Most studies focus on individual lysins or domains, overlooking adjacent full-length endolysin genes. Our large-scale analysis of 21k phage genomes revealed this hidden trend and a possible unrecognised lysis strategy hiding in plain sight.

Plan: We will begin with phage AA002, which infects Staphylococcus hominis, a contributor to human body odour. We 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, we 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.

Impact: 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. In Ferreira’s lab, we host 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. We are currently exploring the contribution of different dermal populations to this fibrosis-free wound healing. Unexpectedly, we found that spiny dermal fibroblasts have a highly plastic phenotype and are able to convert to many other cell types (neurons, myocytes, chondrocytes). Moreover, we found that spiny fibroblasts secrete factors that enhance migration and proliferation of human dermal fibroblasts and protect them from cellular senescence. We aim 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, we aim 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

Discovery: Organisms are continuously bathed in a rich milieu of olfactory compounds. Defined by their ability to elicit our 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. Our 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.

Plan: To explore our serendipitous finding, we will combine in vivo models of skin inflammation with our expertise in multiomic analyses of hidradenitis suppurativa (HS) and pyoderma gangrenosum (PG) patient tissues. We 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.

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

Grant category: Serendipity Grants

Year: 2025

Geography: Denmark

Vision: “Stretch-mediated tissue expansion” is used to grow extra skin during breast reconstruction. We used a mouse model mimicking this clinical process to unravel fibroblast-epithelial crosstalk supporting keratinocytes self-renewal. Unexpectedly, we 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 is unclear. In light of this serendipitous discovery, we now plan to investigate how Schwann cells contribute to the regeneration and re-innervation of peripheral sensory neurons in stretched skin.

Plan: The new project – SkinSense – will explore how stretching affect peripheral sensory neurons and Schwann cells, which are key to skin sensation. We will use single-cell transcriptomics and high-resolution imaging to study how peripheral sensory neurons are affected in terms of structure, function, and repair. Based on these findings, we will test gene therapy approaches using adeno-associated viruses to restore nerve function and recover skin sensation.

Impact: 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.

Grant category: Serendipity Grants

Year: 2025

Geography: Canada

Discovery: We unexpectedly discovered that deleterious TCF3 mutations cause a severe form of atopic dermatitis (AD) associated with inflammatory bowel disease (IBD). By querying large-scale genetic repositories, we also observed that common TCF3 alleles are associated with susceptibility to AD and IBD in the general population. TCF3 encodes a transcription factor that plays a key role in T cell differentiation. Thus, we hypothesize that TCF3 mutations cause abnormal T cell activation, leading to skin and gut inflammation. Given severe AD is a risk factor for IBD, we further propose that the study of TCF3 mutations will shed new light on mechanisms that may underpin both conditions. Plan: The aim of our study is to validate the involvement of TCF3 in the pathogenesis of AD and IBD. This will be achieved by identifying the immune pathways that are altered by TCF3 dysfunction in skin and gut. Thus, our plan integrates: i) in-vitro studies to determine the impact of TCF3 mutations on protein function ii) immune phenotyping of T cells from individuals harbouring TCF3 mutations iii) in-silico analyses to define transcriptional networks driven by TCF3 Potential impact: We expect that our work will identify TCF3-dependent pathways contributing to AD and IBD pathogenesis. This will shed new light on shared disease mechanisms with potential to inform targeted treatment of individuals affected by both conditions.