Xiang Li
Master of Biological Sciences (M.Sc.), Medical College of Wisconsin, USA, 2006
Molecular interactions of pathogens in respiratory cells in modulation of innate immune responses during pulmonary bacterial infections.
Pseudomonas aeruginosa causes pulmonary infections particularly in immunocompromised individuals or patients with cystic fibrosis (CF). CF patients are highly susceptible to P. aeruginosa infections, developing chronic lung infections that result in fibrosis and destruction of lung tissue, and finally die. The mechanisms by which P. aeruginosa cause chronic lung infections are complex, and may at least partially be due to the suppression of host defense systems in the lung. Alveolar macrophages serve as the first line of host defence to clear extracellular bacteria from the lung. In addition, these lung-resident macrophages are critically involved in coordinating the innate immune response during the bacterial infection. Alveolar macrophages are known as long-lived tissue cells with a low incidence of constitutive apoptosis. Therefore, modulation of macrophage lifespan is an important mechanism for regulation of macrophage function and the host defense system. At present, the role of alveolar macrophage apoptosis in the context of CF is not known. My current research is focused to define the molecular mechanisms that regulate the cellular apoptotic response of alveolar macrophages upon P. aeruginosa infection.
1st supervisor: Prof. Dr. Erich Gulbins Institute: Telephone: +49 (0)201 - 723 - 3687 |