SUND Collaborates projects 2025

Chronic autoimmune diseases (AID) such as Sjögren’s disease (SjD) and multiple sclerosis disproportionately affect women, with risk and severity increasing with age. This vulnerability may be linked to immune ageing (immunosenescence), a decline in immune tolerance and age-related changes in female sex hormones.

SjD is a prototypical AID, characterised by inflammation and dysfunction of exocrine glands, primarily salivary and lacrimal glands. Dry mouth, dry eyes, fatigue, joint pain and other organ involvement impact overall health and quality of life. The cause is unknown but thought to involve interactions of hormones, genetics, and environmental triggers. SjD mainly affects women (90%) and is often diagnosed around menopause, highlighting a role for sex hormones. While reduced steroid hormone levels have been reported, the molecular mechanisms by which sex steroids regulate immunity and target organs remain unclear.

This project aims to clarify endocrine mechanisms driving pathogenic immune responses and loss of tolerance, using SjD as one of the models. We will measure sex steroid levels and inflammatory mediators in blood and saliva, assess sex steroid receptor expression and steroid production in salivary glands. These findings will be integrated with clinical and paraclinical features to determine how altered sex steroid signalling shapes immune responses and disease manifestations.

This pioneering multidisciplinary consortium at the Faculty of Health and Medical Sciences brings complementary expertise within SjD research, autoimmune regulation and discovery of FoxA1+ regulatory T cells and steroidogenesis to advance the project. On the long-term, this will generate novel and deeper understanding of the cellular and molecular pathways regulated by sex steroid receptor signalling in immune cells, their variations through the different cycles in a lifespan and associated risk of autoimmunity in women, and open avenues for novel targeted treatments in autoimmunity.

Antimicrobial resistance is a critical global health threat that requires a One Health approach to capture the interconnected risks across humans, animals, and the environment.

While the role of antimicrobial use in medicine and agriculture is well established, environmental drivers of antimicrobial resistance remain poorly understood. In particular, fine particulate air pollution (PM2.5) has been largely overlooked, despite its potential to act as a vector for resistant bacteria and antibiotic resistance genes, to create selective pressures that foster resistance, and to alter host susceptibility, thereby influencing infection dynamics.

We propose to establish the GAIA consortium to address this gap by integrating molecular geobiology, medical microbiology, environmental epidemiology, and geochemistry.

Our research has three objectives:

• Determine how aerosol particles influence bacterial mutagenesis and AMR gene uptake.
• Assess the association between long-term PM2.5 exposure and AMR incidence in the Danish population using nationwide surveillance and register data.
• Quantify how particle-associated biofilms shape lung infection outcomes and treatment responses in vivo.

Through this combination of fundamental and translational research, we aim to generate robust mechanistic and epidemiological evidence for the role of air pollution in antimicrobial resistance propagation.

The GAIA consortium further provides a platform for interdisciplinary collaboration and expansion into related areas, including antimicrobial resistance propagation in the plastisphere, environmental transmission in livestock settings, and mitigation strategies in countries with high air pollution burdens. By bridging discovery science, epidemiology, and clinical research, we will provide critical insights into the overlooked environmental dimension of antimicrobial resistance and lay the foundation for new preventive and therapeutic solutions.

Could infections in the brain be the missing link in psychiatric illness? Mental health disorders are a leading cause of global disability, yet their biological origins remain poorly understood. While research has centered on neurotransmitters such as serotonin and dopamine, growing evidence points to infection and immune response. Before antibiotics, syphilis invading the brain (neurosyphilis) caused by Treponema pallidum accounted for one-third of psychiatric hospitalizations, and its treatment with penicillin remains a clear example of infection driving mental illness. Today, epidemiological studies show infections and immune disturbances increase the risk of schizophrenia, depression, and other disorders, but direct molecular studies have been limited by lack of suitable material.

This project leverages the Danish Brain Collection, the world’s largest archive of brains from psychiatric patients (1945–1982), when neurosyphilis was prevalent, to establish proof-of-concept for infection-based models of mental illness.

Using advanced molecular and imaging tools, the project will:

• Identify pathogens in archived brain tissue.
• Link these findings to clinical records and immune activation patterns.
• Assess how immune activation relates to psychiatric symptoms.

In parallel, the project embeds ethics, since the collection was assembled without consent standards. Together with ethicists, clinicians, patient representatives, and museums, we will engage the public through debates, podcasts, and exhibitions. Additionally, the project will establish a new interdisciplinary position in neuroinfection at SUND, linking psychiatry, infection biology, pathology, and ethics.

By reframing psychiatric disease as partly systemic and biological, the project may reduce stigma while opening pathways to new diagnostic markers and therapies. It will engage the public on the ethics of using archival material, ensuring marginalized patients from the past continue to educate the living and shape future mental health care.

This collaborative research project is focused on the role of extracellular matrix (ECM) remodelling as a potential “molecular memory” of obesity, exploring how structural changes in ECM contribute to long-term metabolic regulation and tissue plasticity in humans and rodents. Obesity imprints persistent alterations across various tissues, yet the mechanisms underlying these enduring changes remain elusive. Our core hypothesis is that ECM remodelling encodes a lasting, molecular signature of obesity. To probe this, the project will generate a comprehensive cross-species atlas encompassing ECM composition, architecture, and mechanics in lean versus obese states, with stratification by sex.

The project combines a human intervention study recruiting obese and healthy controls for tissue biopsies, metabolic assessments before and after prolonged fasting — with parallel rodent diet-induced obesity models. These models enable controlled mechanistic studies on ECM and glycocalyx alterations, assessed via advanced glycomics, proteomics, and imaging techniques. Particular focus is dedicated to the adipocyte and endothelial glycocalyx - a specialized carbohydrate-rich layer vital for cellular function.

The project will map glycocalyx composition and structural changes to understand how ECM and glycocalyx remodelling impact vascular and metabolic health. The overarching goal is to identify structural and molecular signatures that underpin the persistent metabolic risks associated with obesity. A long-term goal is to identify biomarkers and therapeutic targets to “reset” ECM states, potentially improving the durability of weight loss and metabolic health.

This collaborative project emphasizes training the next generation of researchers, fostering collaborations across disciplines, and establishing open resources for the scientific community. This project integrates researchers at SUND which combine forces to provide cutting edge research from bedside to bench.