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In addition to their function as energy carriers, metabolites of our food also have a role as direct modulators of immune functions. Immune responses require changes in our metabolism, conversely, immune responses also dictate changes in our metabolism. The aim of our research group is to study the interplay of immunology, metabolism and nutrition to contribute to the prevention and resolution of inflammation in autoimmune diseases.


Influence of short-chain fatty acids on autoimmunity
Short-chain fatty acids (SCFA) are metabolites of our intestinal bacteria that are produced when fiber is converted. Preventive treatment with SCFA has a protective effect on the development of inflammatory diseases such as RA, but the influence of SCFA on already established inflammatory processes is largely unknown. We investigate the impact of SCFA propionate on RA resolution. Here we analyze the effect of propionate supplementation on the intestinal flora and its released metabolites and how these can alleviate ongoing inflammatory processes. Our goal is to gain a better understanding of the connection between intestinal flora and inflammation and to establish new, nutrition-related therapy options for inflammatory diseases such as rheumatoid arthritis.


Intestinal post-translationally modified proteins and their potential to induce rheumatoid arthritis (RA).
We investigate how modified gut proteins are involved in the early appearance of modified protein antibodies (AMPA) responsible for synovial inflammation in arthritis. Modified proteins can act as novel antigens and provide the basis for early autoantibody production that later cross-reacts with local tissue antigens in the joints, promoting disease onset and disease severity. Therefore, we aim to clarify the role of AMPA in synovial inflammation in RA. It is expected that our findings can be directly applied to novel treatment strategies in emerging RA.


Influence of dysbiosis on the intestinal barrier
Dysbiosis of the gut microbiome and a defect in the gut barrier represent a risk factor that can lead to the development of autoimmune diseases such as RA. Mice with collagen-induced arthritis show a change in the intestinal microbiome and increased permeability of the intestinal barrier even before the onset of symptoms. We therefore assume that changes in the composition of the intestinal bacteria and the resulting metabolic products cause changes in the intestinal barrier. This project deals with the question of which early changes in the intestine are involved in the development of arthritis.


Alcohol modulates immune responses
It has long been known that moderate to heavy alcohol consumption reduces the severity of autoimmune diseases, but at the same time reduces the effectiveness of vaccination. Unfortunately, specific cellular or molecular mechanisms by which alcohol modulates the immune system are poorly understood. Recently, we uncovered cellular mechanisms by which acetate, the metabolite of alcohol, reduces helper T cell responses. We are currently investigating molecular mechanisms in T cells that are directly responsible for decreased T cell function as a result of increased alcohol exposure.


Relationship between intestinal inflammation and bone loss - what role does the hormone erythropoietin play?
Severe bone loss in patients with rheumatoid arthritis is often accompanied by intestinal inflammation. In contrast, patients with chronic inflammatory bowel diseases have an increased risk of developing osteoporosis and osteopenia. Against this background, we are investigating the connection between intestinal inflammation and the development process of arthritis. We also want to specifically investigate the effects of erythropoietin (EPO), a hormone that is mainly released in the kidneys and stimulates the production of red blood cells. In addition, EPO also has effects on other cells, sometimes on the intestinal endothelium - i.e. cells lining blood vessels - and osteoclasts (bone-degrading) and osteoblasts (bone-building progenitor cells). Thus, EPO could be a central link between bone loss and intestinal inflammation.


BTN in T cell activation
Together with B lymphocytes, T cells form the adaptive arm of the immune system. Many autoimmune diseases, such as rheumatoid arthritis, multiple sclerosis or systemic lupus erythrematosus, are characterized by unwanted T cell responses against endogenous characteristics. In healthy people, the activation of such T cells is suppressed by a wide variety of tolerance mechanisms. We investigate the influence of butyrophilins (BTNs), a group of co-stimulatory molecules, on T cell activation, both during maturation in the thymus and on peripheral T cells. Using genetic "knockout" models, we want to characterize how BTNs contribute to preventing this tolerance breach and test possible therapeutic approaches with co-inhibitory BTNs.


Role of lymph node scaffold cells in regulation of immune response
Previously considered primarily as scaffolding cells to facilitate the meeting of B, T, and dendritic cells (DC), lymph node stromal cells (LNSC) have recently attracted more attention for their demonstrated ability to actively regulate immune cell functions drawn. Here we are interested in investigating the role of a particular LNSC subset, the fibroblastic reticular cells (FRC), specifically in the popliteal lymph nodes (pLN) during the initiation of RA.


Publications

Our publications on PubMed

Videos & Media

PODCAST:


Nutrition is the key to everything...

Listen to the Podcast of Dr. Anne Fleck, one of the best-known and most unconventional nutritionists in Germany, explaining the link between nutrition and the development of disease.


Dr. Anne Fleck - Gesundheit und Ernährung mit BRIGITTE LEBEN! | AUDIO NOW


ARTICLES & VIDEOS:

Team

  • Alumni

    Vugar Azizov, PhD

    Carolin Brandl, PhD

    Magarete Schimpf, MTA

    Ippei Miyagawa, MD/ PhD

    Michael Frech, PhD

    Michel Hübner, M.Sc.

     

    Catarina Schneider, M.Sc.

     

    Fabian Schälter, PhD

    Agnus Monica Davis, M.Sc.

    LabLife

    Contact

    Prof. Dr. Mario M. Zaiss

    Friedrich-Alexander-University Erlangen-Nürnberg (FAU),

    Universitätsklinikum Erlangen, 

    Department of Internal Medicine 3 - Rheumatology and Immunology

    Glückstrasse 4a,

    D-91054 Erlangen,

    Germany


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