Markus Bosmann, M.D.
Assistant Professor of Medicine
Graduate School: Johann Wolfgang Goethe-University, Frankfurt a. M., Germany
Fellowship: University of Michigan, Ann Arbor, MI (Peter A. Ward, Department of Pathology)
- Acute respiratory distress syndrome (ARDS)
- Bacterial sepsis
- Lung fibrosis
- Infection-associated inflammation
- Host-pathogen interactions
- Innate immunity
- Macrophages, neutrophils, T cells, lung epithelial cells
- Cytokines (e.g. IL-27/IL-27RA)
- Complement system (e.g. C5a/C5aRs)
- Signaling pathways (e.g. MAVS)
- Gene editing (CRISPR/Cas9)
Sepsis and acute respiratory distress syndrome (ARDS) are life-threatening diseases and frequently require treatment in critical care medicine. Patients with bacterial pneumonia are under increased risks for the development of both ARDS and sepsis. There are estimated more than 600,000 annual cases of sepsis and ARDS in the United States. In the current absence of FDA-approved drugs, the mortality rates of ARDS and sepsis remain around 20-50%. Hence, these disorders represent important clinical problems with an urgent need for a better understanding of their pathogenesis.
Accumulating evidence suggests key roles of dysbalanced innate immune responses, inflammation and host-pathogen interactions during pneumonia, ARDS and sepsis. The presence of pathogen-associated molecular patterns (PAMPs) provokes the release of a plethora of inflammatory mediators (e.g. cytokines, complement anaphylatoxins) accompanied by complex interactions of intracellular signaling cascades. The focus of our experimental research projects is on the cellular and molecular mechanisms of these innate immune responses including macrophage functions, neutrophil extracellular trap (NETs) formation, cytokines/chemokines, complement, signaling pathways and novel bacterial PAMPs (e.g. polyphosphates). We employ transcriptome-wide screening approaches (RNA-Seq.) for identifying novel differentially expressed genes in experimental sepsis/ARDS and are experienced in generating new transgenic mouse models (e.g. Cre-lox, CRISPR/Cas9). In summary, our studies aim for a better understanding of the molecular pathogenesis of infection-associated inflammation during sepsis and ARDS, thereby helping to identify future avenues for therapeutic interventions.
Please see BU Profile for complete Publications list
- The inflammatory response in sepsis
- Extracellular histones & neutrophil extracellular traps
- Experimental ARDS