all staff members
Dr. rer. nat.
Monika Heiner
scientific lab manager
Dr. rer. nat.
Barbara Sprenger
scientific administrator
Dr. rer. nat.
Corinna Bremer
scientific administrator KFO 309
Sandra Rinnert
Laboratory Veterinarian
Post Docs
Ivonne Vazquez-Armendariz , PhD
Christin Peteranderl , PhD
Irina Kuznetsova , PhD
Dr. biol. hom.
Learta Pervizaj Oruqaj
Dr. rer. nat.
Lucie Sauerhering
Dr. med.
Ulrich Matt
,
PhD
Balachandar Selvakumar , PhD
Dr. med.
Lucas Kimmig
Visiting Scientist
PhD students
Christina Malainou , MD
Bacterial superinfection after influenza virus (IV)-induced lung injury significantly contributes to disease severity and mortality. The pathogenesisis characterized by mutual interactions between the co-infecting pathogens and the host. One important mechanism is the depletion of a specific subset of lung macrophages called resident alveolar macrophages (rAM), which act as first line innate immune defense by phagocytosing invading bacteria in the alveolar space. rAM death in vivomay be driven by both the viral infection itself and host-derived inflammatory signals. Currently, the respective contribution of these processes and the downstream signaling pathways involved are largely unresolved. Aim of this project is to characterize infection-induced death pathways in rAM, develop strategies to inhibit them and restore rAM function as well as assess the effect of rAM protection/restoration on a bacterial superinfection level.
Margarida Barroso , M.Sc.
Julian Better
Antimicrobial properties of alveolar macrophages during resolution of Inflammation Acute lung injury (ALI) is caused by direct or indirect insults to the lung, and is associated with high morbidity and mortality. Bacterial superinfections are feared complications of ALI. On the cellular level, alveolar macrophages are key innate immune cells that initiate and resolve an inflammatory process. Resolution of inflammation might impair the macrophage´s ability to clear bacteria, thus predisposing to superinfections. My project focuses on the kinetics and activation state of macrophages/monocytes during ALI in the context of bacterial superinfections
Theresa Schäfer
The role of GM-CSF in stem cell-driven alveolar repair following influenza virus infection Inflammation resolution and stem cell mediated repair of the distal lung tissue is crucial for outcome of Influenza A virus (IAV)-induced lung injury. The Granulocyte-macrophage colony-stimulating factor (GM-CSF) is an important mediator of lung regeneration. The aim of my PhD work is to elucidate the role of GM-CSF-dependent signaling in protection and repair of the distal lung epithelium after IAV infection and to identifie the compartment of the stem cell niche in which GM-CSF is induced during IAV infection. A further aim is to elucidate which cell and downstream effector mechanisms are mediating the different steps of GM-CSF-dependent lung tissue repair and injury prevention.
Ludmilla Sperling
parental leave
MD students
Julia Bespalowa
Dorgeline Blanche Nganko
Martin Langelage
Anna-Lena Ament
Master student
Marie Rupp
Master student
Non-scientific staff
Larissa Hamann
technician
Stefanie Jarmer
technician
Florian Lück
technician
Corinna Plate
technician
Nicole Tewes
study nurse
Han-Le Nguyen
student assistant
Alumni
Jennifer Quantius , PhD
Dr.
Carole Schmoldt
Lina Jankauskaite , MD, PhD