부산대학교 도서관

In order to gain a better understanding of the mechanisms controlling inflammatory processes with a view to developing novel therapies for inflammatory disease, the research presented in this thesis has been focused on unravelling the molecular complexities associated with the initiation, propagation and resolution of inflammation. Although neutrophilic and eosinophilic granulocytes are key effector cells in orchestrating host defence against invading bacteria and parasites, their over-recruitment, uncontrolled activation and defective removal by macrophages play a prominent role in generating tissue damage associated with chronic inflammatory conditions such as asthma and rheumatoid arthritis. Much of the work presented in this thesis investigates these processes and the findings are divided into three overlapping sections; initiation, propagation and resolution of the inflammatory process. Section 1 describes studies principally investigating the mechanisms governing the initiation and regulation of the inflammatory process. The main focus of this section involves work investigating the activation and responsiveness of neutrophils, eosinophils, macrophages and platelets to agents such as various lipids, small peptides and nitric oxide. Section 2 presents publications describing the propagation of the inflammatory process in various in vivo models of skin and lung inflammation including studies investigating relevant in vitro inflammatory processes. Section 3 describes research focusing on the processes governing the resolution of inflammation especially the phenomena of apoptosis and macrophage clearance of apoptotic cells. This includes in vitro studies investigating the mechanisms regulating human granulocyte apoptosis and in vivo work investigating the effects of apoptosis modulation in different models of inflammation.