Since the first gene transfers into mice in 1980, transgenic mice have allowed researchers to study the role of genes in development, physiology and disease. In this module participants will have the opportunity to get an introduction into current technical possibilities (Figure Purkinje-cell specific disruption of Kcc2). In this module several mouse models for hereditary human disorders from our currently ongoing scientific projects will be presented. Practical work will include molecular biology including cloning strategies and genotyping techniques. You will also have the possibility to get insights into mouse embryo manipulation. Selected initial mouse phenotyping techniques will be demonstrated including morphological techniques, behavioral analysis, and electrophysiology.

Staining of cerebellar sections from wild-type (WT, left) and Purkinje cell specific Kcc2 knockout mice (KO, right). Kcc2 is stained in green, Purkinje cells are labelled in red for calbindin and nuclei are stained with DAPI in blue. In the cell specific KO Purkinje cells do not express Kcc2 any more, while Kcc2 expression in granule neurons and interneurons is preserved.

Pneumolysin (PLY) is a major virulence factor of Streptococcus pneumoniae and crucial for the pathogenesis of invasive pneumococcal disease and sepsis following community-acquired pneumonia (CAP). The β-pore-forming toxin recognizes membrane cholesterol leading to disintegration of the alveolar epithelial barrier and impairment of innate immunity. Remotely, pneumococcal CAP triggers a hepatic activation of the sterol biosynthesis through a yet unknown mechanism that depends on PLY in mice. Supplementation of cholesterol species or delivery of cholesterol by polymer nanoparticles is evaluated as a candidate for adjuvant therapy to counteract pore formation. PLY may be seen as a homeostasis-altering molecular pattern (HAMP) as it directly activates key regulators of the lipid homeostasis resulting in a rapid increase of cellular cholesterol. Some of these effects may be the result of inflammasome-signaling activated through PLY-pore stress. Inflammasome signaling partly contributes to cell death in pneumococcal diseases but on the other hand may also alter the lipid homeostasis, increasing lipid and particular cholesterol biosynthesis. Together we will investigate the nature of the PLY-activated sterol biosynthesis to decipher its relevance in the pathophysiology and survival of life-threatening infections applying molecular and functional assays on cell lines stimulated with bacterial toxines.

Figure: Two-photon microscopy of the Pneumolysin (PLY) induced cholesterol biosynthesis using Filipin III staining to quantify cellular sterols in HepG2 cells.

Air pollution poses a growing global health challenge, with fine particulate matter (PM) contributing substantially to the burden of respiratory diseases and premature death. PM exposure is closely linked to chronic respiratory diseases and increases susceptibility to respiratory infections by compromising epithelial integrity and weakening innate immunity. Influenza A viruses (IAVs) are among the most relevant respiratory pathogens and can cause severe and sometimes life-threatening lung diseases, particularly in vulnerable individuals. Recent findings suggest that PM may further exacerbate the severity of viral infections. However, the molecular mechanisms influencing pathogen load, host cell homeostasis, and immune regulation remain poorly understood. Building on an established in vitro infection model for IAVs, current studies are investigating PM-mediated modulation of pathogen-host interactions, focusing on virus-induced signalling pathways, inflammatory responses, and cell death mechanisms.

During the summer school, participants will contribute to ongoing experiments with cellular infection models, both with and without exposure to environmental pollutants. The training includes sterile cell culture techniques under BSL-2 conditions, as well as the practical application of methods such as plaque titration and Western blot analysis.

Musculoskeletal disorders have been the main reason for incapacitated days for years. Our group's research focuses on musculoskeletal disorders that result in dysfunction, pain and disability. Our goal is to elucidate the mechanisms that affect tissue degeneration and regeneration, with particular attention to bone, tendon and cartilage tissue. We are also interested in optimizing materials / implants to reduce the risk of material-related infections, which are serious complications in orthopedic surgery. For our studies we use human tissue and cells as well as the material from well-defined animal models. The main methods used in the various projects include gene expression analysis, protein assays, histology and immunohistochemistry, various cell culture models and a set-up for mechanical stimulation of cells in vitro. During the practical period, the student is involved in one of the ongoing projects and carries out a small project under the supervision of a team member.

1. Borcherding at al. Materials 2019; doi:10.3390/ma12233838
2. www.flexcellint.com

Sex differences have been described in kidney diseases such as diabetic nephropathy (DN) as well as in age-associated kidney damage. In our research group, we are mainly interested in 2 proteins that play a role in these sex differences. These are the non-fibrillar collagen type VIII and the scaffold protein MORG1, of which we know from our animal studies that their renal expressions are dependent on the factors diabetes, age and sex. In our current projects, we are trying to understand the underlying molecular mechanisms. To this end, we are working at different levels: 1) with cell lines, 2) ex vivo with pieces of kidney tissue, 3) with material from mice and 4) with human material. Our range of methods is very diverse and includes common molecular biology techniques (siRNA experiments, real-time PCR, Western blot) and various staining techniques (histochemistry, immunohistochemistry and OPAL-based multiplex immunofluorescence staining).  

The human skin is a highly dynamic immunological organ that integrates barrier function, tissue repair, and tumor surveillance. This module introduces advanced human in vitro model systems to dissect the complex interplay between skin cells, immune responses, and tumor development, with a particular focus on human biology, immunology, and cutaneous malignancies.

Participants will explore 2D and 3D human skin models developed from primary keratinocytes and fibroblasts to study viability, apoptosis and inflammatory signaling. Fully human 3D full-thickness skin equivalents recapitulate dermal–epidermal crosstalk and allow controlled modeling of infection, inflammation, and tissue regeneration. Disease-specific models of psoriasis and atopic dermatitis have been generated through Th1- and Th2-cytokine stimulation, enabling transcriptomic and morphological characterization of inflammatory phenotypes and therapeutic responses.

A central focus of the research group is the metabolic regulation of the human immune response. Using omics-based approaches in fully human systems, we investigate macrophage immunometabolism in non-infectious granulomatous skin inflammation. Our work has identified a linear macrophage signaling axis linking Th1-driven immune activation to metabolic reprogramming required for granuloma formation, revealing important deviations from canonical paradigms derived from animal models.

Building on this expertise, we examine the crosstalk between T-cell immunity and the tumor microenvironment in cutaneous squamous cell carcinoma and malignant melanoma. Metabolomic analyses of patient-derived samples demonstrate tumor-specific metabolite accumulation with direct immunosuppressive effects on T cells. To functionally model these interactions, we are developing immune-competent 3D melanoma skin models, enabling real-time optical monitoring.

Ageing is a biopsychosocial process: physical function, cognition, mood, social support, and care structures interact and jointly shape health, resilience, and independence in later life. This Summer School offers medical and health-related students a compact, research-oriented introduction to modern geriatric medicine and health services research at Jena University Hospital.

The core focus is how “biopsychosocial hallmarks of ageing” can be assessed, measured, and interpreted in real-world geriatric care. Participants will be introduced to key geriatric assessments and patient-reported outcome measures (PROMs), and will receive a practical introduction to psychometric concepts (e.g., scale properties, reliability, missing data) and basic statistical analysis of geriatric datasets. A major emphasis is placed on clinical interpretation: how can assessment results inform patient-centered care, vulnerability profiling, and care planning?

The course combines clinical exposure with structured scientific work. Depending on language skills and prior experience, students will either contribute to supervised assessment-based clinical observation or work with curated anonymized datasets and case vignettes. This enables meaningful and scientifically equivalent participation for both German-speaking and international students. Typical topics include function and mobility, frailty, psychosocial burden, quality of life, and care pathways in older adults.

Designed as a one-week intensive format for small groups (1–2 students), the Summer School allows close supervision and direct interaction with the geriatric team. By the end of the week, participants will present a short data-based project, including methods, results, and a clinical/health services interpretation. The program is particularly suited for students interested in geriatrics, patient-centered outcomes, health services research, and the interface between clinical medicine, measurement science, and data analysis.