Udforsk vores bevillinger og priser

Grant category: Research grants in open competition

Årstal: 2020

Lande: Denmark

Atopic Dermatitis (AD) is a common inflammatory skin disease affecting 15% of children and 3-5% of adults. AD is associated with the risk for developing co-morbidities such as other atopic diseases (food allergy, asthma, and rhinitis) and infections. Co-morbidities are believed to occur because of functional changes in the immune system of AD patients, however, it remains unknown how these changes are established. Emerging experimental studies suggest the existence of a skin-gut immune axis, but the role for the gut remains largely unexplored in AD.

The goal of this project is to determine if AD changes the bacterial microbiota composition and function in the gut, alters the intestinal and systemic immune system, and increases the risk for food allergy co-morbidity via oral sensitization. The project hypothesizes that AD drives dysregulated immune responses to the gut microbiota, which in turn changes the immune system giving rise to atopic co-morbidities and risk for infections. In other words, it is envisaged that AD patients become “allergic” to the bacteria present in their intestine – leading to a “persistent allergic reaction” due to continuous presence of bacteria in the intestine.

The project will use a rat model of AD to investigate the hypothesis and perform a human case-control study to support the clinical relevance of the findings. Identification of bacterial drivers of persistent type-2 inflammation could open new avenues for the prevention and treatment of AD and related co-morbidities.

Grant category: Research grants in open competition

Årstal: 2020

Lande: Canada

Cutaneous leishmaniasis (CL) is a designated ‘WHO top-neglected tropical disease’, with up to 1 million new cases worldwide annually. CL is an inflammatory skin disease caused by infection with Leishmania parasites that leads to tissue damage, ulcers, and severe scarring, despite current treatment options.

The goal of this project is to provide a key rationale for pursuing Granzyme B (GzmB) as a novel therapeutic target for the treatment of cutaneous leishmaniasis. 

GzmB is a protein that is aberrantly elevated in CL lesions and other inflammatory skin conditions. GzmB activity has been demonstrated to cleave important proteins in the skin, thereby worsening tissue damage, delaying wound healing, and causing scarring in inflammatory patient skin specimens and in experimental models. Importantly, inhibition of GzmB has shown efficacy in delaying these disease phenotypes.  

Using lesional specimens from CL patients, a well-established experimental model, and a GzmB inhibitor, the contributions of GzmB to inflammation, impaired wound healing, and scarring in CL will be delineated in this study.