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Infection and Immunology

Term: 01.09.2020 – 31.08.2021

Molecular ultrasound of inflammatory bowel disease has not yet been established. We want to exploit the essential role of endothelial cell adhesion molecules in the development of colitis and establish CAM (cell adhesion molecule)-specific ultrasound contrast agents in DSS-induced murine colitis for the analysis of colonic inflammation. This will facilitate both, assessment of disease progression and treatment response monitoring.

Term: 01.05.2020 – 30.04.2021

Systemic sclerosis (SSc) is a prototypic fibrotic disease, with TGF-beta as a key mediator of fibroblast activation. Engrailed-1 (EN1) identifies a fibroblast lineage with intrinsic fibrogenic potential. We showed that EN1 was upregulated in fibrotic skin by TGF-beta, and that EN1 knockout partially prevented fibroblast activation and fibrosis. Next, we aim to study EN2 in fibrosis, to evaluate how EN1 is upregulated and to provide further evidence for the role of EN1 in fibroblast activation.

Term: 01.09.2020 – 31.08.2021

One third of the depressed patients do not respond adequately to conventional treatment. This seems to be associated with increased production of proinflammatory cytokines such as TNF-a and IL-1, as well as dysregulation of cortisol levels. This project aims to investigate the impact of the new psychotherapeutic method TaKeTiNa on serum lipids, cortisol Levels, and the production of proinflammatory cytokines.

Term: not started yet

Osteoclasts are the bone-resorbing cells of the body, which lead to severe damage of the musculoskeletal system under pathological conditions (such as RA). Treatment with soluble CD83 inhibited bone destruction in the murine arthritis model. Aim of this proposal is the translation of the murine data into the human system, which repre-sents the next important step towards future therapeutic applications.

Term: not started yet

Intestinal barrier integrity is an important checkpoint in translating autoimmunity to inflammation in rheumatoid arthritis (RA). Microbial metabolites of tryptophan were shown to reduce intestinal permeability and inflammation. However, it is unknown if this translates to a favourable impact on RA. Furthermore, it is unknown how the metabolites are intestinally resorbed. These questions should be adressed in cell models of intestinal epithelium and in human serum samples.

Term: Not started yet

Basic research focusing on TCs differentiation might contribute to the understanding of pleiotropic immune functions of the intestinal epithelium, which can be exploited in the context of immunomodulation. Our preliminary data support an interplay between type2 cytokines and Rac1/RhoA function within IECs playing a role in the differentiation of IECs towards a TCs fate. Our aim is then to decipher the molecular mechanisms operating behind intrinsic/extrinsic control of TCs cell fate decision.

Term: Not started yet

T cells are an integral part of adaptive immunity, which forms the basis of protection from infections after vaccination. While B cell and antibody responses are well understood, little is known about which antigen-reactive T cells are recruited after primary and booster vaccination, as well as into long-lasting resting memory. In this project, we will investigate these questions in SARS-CoV-2 vaccinees by state-of-the-art T cell receptor repertoire profiling and functionality assessments.

Term: not started yet

In patients with periodontitis, orofacial clefts and partly also during orthodontic treatment an oral dysbiosis and an increase of inflammation markers have been observed. Here, for the first time a systematic analysis of the oral microbiome and local inflammation in oral niches will be carried out using 16S rDNA sequencing and multiplex immuno assay, which will be correlated with determinants such as gingivitis/periodontitis, age, orofacial clefts, exogeneous factors and orthodontic treatment.

Term: Not started yet

Trauma is the leading cause of death in humans aged below 45. Trauma can affect everyone, everywhere at any time. Blunt cardiac injury is associated with increased mortality after trauma. Redistribution of the gap junction protein Connexin43 is associated with cardiac dysfunction. In the present project, important new molecular insights into the regulation of Cx43 in the heart after trauma will be revealed and may identify therapeutic targets for preservation of cellular coupling.