Due to their physiological functions our mucosal surfaces are in direct contact to the environment and thus represent the major port of entry for pathogens. To protect the body from severe infections an effective mucosal immune system is indispensable. We are studying respiratory tract infections with the focus on influenza and pneumococci, which represent the most frequent viral and bacterial infectious agents for pneumonia in humans. A major focus of our research is to study molecular and cellular processes during coinfection with influenza and pneumococci and here in particular the immunological functions of the alveolar epithelium in host defense.
Lower respiratory tract infections belong to the most frequent causes of death worldwide and also in Germany. Streptocuccus pneumoniae (the pneumococcus) and influenza represent the most important bacterial and viral causative agent of pneumonia. While both pathogens alone can cause severe courses of pneumonia they can also act together establishing so-called coinfections with fatal outcome. Here, the preceding influenza infection impairs immunity to secondary pneumococcal infection which in consequence cannot be efficiently controlled and thus may enter the blood stream. If untreated, systemic dissemination of the bacterial pathogen (septicemia) induces overshooting and immune responses and death within a short period of time.
Using mouse infection models to study the underlying mechanisms for enhanced susceptibility to bacterial coinfection following influenza the major focus of our research is to decipher in very much detail the immunological functions of the alveolar epithelium, particularly the type II alveolar epithelial cells (AECII). In previous studies we have shown that AECII exhibit important functions not only in the induction but also the regulation of adaptive immunity. Moreover, we demonstrated that in the early phase of influenza infection AECII act as a kind of integrative unit that integrates pathogen-derived danger signals and inflammatory signals derived from other lung sentinel cells and exhibit crucial functions in the initiation of antiviral immunity in the lung. Based on these findings we currently study how preceding influenza infection alters the immunological response of AECII to pneumococci and to what extend this may contribute to the dysregulated immune response to secondary bacterial infection following influenza.
We have previously shown that influenza infection induces lung-term enhanced susceptibility to bacterial pathogens, i.e. even weeks after the virus has been eliminated the immune response to pneumococci is altered. Next to deciphering local virus-induced changes in lung immunity we as well study how influenza pneumonia sustainably alters hematopoiesis of immune cells in the bone marrow. Here we focus on myeloid cells which exhibit crucial functions in the early defense against bacterial pathogens.
Next to using mouse models to study infectious diseases we teamed up with clinicians to study the role of secretory immunoglobulins in the altered immune response to pneumococci in asthmatic patients. Another clinically-oriented project focusses on the only recently described mucosal-associated invariant T cells (MAIT) and their role in age-associated enhanced susceptibility to Clostridium difficile infections in human patients. Further information to the above mentioned projects and a description of additional ongoing research projects can be found here.
Bachelor & Master
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