Abstract
The studies in this thesis show that the observed clinical epidemiology of the CGD host is the results of a unique interaction between the pathogen and the host. The pathogenesis of invasive fungal infections is a continuum between infection and inflammation. Since the NADPH-oxidase complex acts both as an antimicrobial effector molecule and a regulator of inflammation, fungal pathogenesis in patients with CGD is the result of an imbalance of antifungal capacity and regulation of inflammation.
The hitherto accepted view, invasive fungal infections in CGD are the results of a defective antimicrobial function of the NADPH-oxidase, has to be revised following the findings in this thesis.
This research gives us new, important insights in the host-pathogen interaction between filamentous fungi and the CGD host. It opens new perspectives in current treatment possibilities. It emphasizes the role of inflammation in infection diseases and the urgent need to focus on this topic if we want to make miles in the treatment and the survival of children with this devastating primary immunodeficiency.
