Defensins, natural endogenous antibiotics, are effectors of the innate immune system and play a significant role in protecting the host from the invasion of pathogens. An impaired intestinal barrier function is a critical factor in the pathogenesis of ileal Crohn's disease, an inflammatory disease of the intestinal tract but has been also associated with obesity and metabolic syndrome. Previous results revealed that a high-fat and high-sugar diet, so called Western-style diet, can cause epithelial barrier dysfunction. We therefore investigate nutritional factors that might directly modulate the intestinal barrier or influence it through changes in the composition and function of the intestinal microbiota and bacterial metabolites like short chain fatty acids (SCFAs) produced by intestinal microbes. Elucidating the underlying mechanisms involved in the regulation of antimicrobial host defense could help to develop new strategies for future therapeutic interventions with the potential to support the barrier function and thus prevent or treat diseases such as obesity and its related chronic diseases.
Projects
- Functional role of antimicrobial peptides and defensins
- Molecular mechanisms mediating the effects of dietary factors on antimicrobial host defense
- Influence of nutritional factors (sugars, fatty acids, vitamins) on intestinal barrier function
- Role of gut microbiota and its metabolites in shaping host immunity
- Identification of drug targets to sustain innate barrier function: Efficacy of defensins in restoring intestinal barrier function and prevention of obesity
- Effects of prebiotic supplements on intestinal barrier function in diet induced obesity
- Role of the serotonergic system in diet-induced gut barrier dysfunction
- Intestinal 3D organoid cell culture as disease model
Role of antimicrobial host defence in diet-induced intestinal barrier dysfunction and its impact on gut microbiota (Louisa Filipe Rosa).
Therapeutically and preventive effects of defensins on gut microbiota, diet induced intestinal barrier dysfunction and the pathogenesis of hepatic steatosis in C57BL/6J mice.
