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- Translational Research Unit – Infectious Diseases
- Metabolism in host pathogen interactions (AG Fischer)
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- HEnRY
Metabolism in host pathogen interactions (AG Fischer)
Bloodstream infections caused by bacteria often lead to severe clinical disorders in patients, which often suddenly result in life-threating conditions such as sepsis and septic shock. Sepsis continues to cause approximately six million deaths worldwide as it is frequently under diagnosed at an early stage when it is still reversible indicating that reliable biomarkers are missing. Moreover, the global emergence of increasing numbers of multidrug resistant pathogens causing sepsis and the gap of antibiotic therapies are important reasons for high morbidity and mortality. Thus, new concepts tackling infections caused by multiresistant bacteria are highly needed. Recently, targeting the host’s metabolism was identified as a promising strategy to treat infections caused by multidrug resistant pathogens by activating pathways that empower host defense mechanisms. Macrophages are highly plastic cells at the forefront of innate immune response towards infections, which not only function in cellular degradation mechanisms but also integrate signals from metabolic pathways and hormones. The dynamic interplay between metabolism and immune responses in health and disease, by which different immune cells impact on metabolic processes, are being increasingly appreciated. Recently, we have identified different metabolic regulators in response to bacterial infections such as leptin signaling using mouse models, which we now aim to translate into human infectious diseases. Moreover, the diagnostics of multiresistant pathogens relies on blood culture diagnostics or sequencing data until now. However, it takes several days until the results of antibiograms are available to adapt the treatment in patients facing infections due to multiresistant pathogens. Here biomarkers, which could detect patients at risk for infections with multiresistant pathogens would close the gap until the data of antibiograms is available. In our group we aim to study the impact of metabolism in host-pathogen interactions to identify new therapeutic strategies targeting multiresistant bacterial infections.