Regulation and mechanisms of resistance to anti-inflammatory mediators in a mouse model of malaria-associated acute respiratory distress syndrome.

Several anti-inflammatory mediators (AIMs) tightly regulate immune responses to pathogens in order to avoid immunopathology. Their production is considered as a major layer of the regulation of inflammatory processes. In this project, we will explore the sensitivity vs resistance to these AIMs as a new layer in the regulation of inflammation. Our mouse model for malaria-associated acute respiratory distress syndrome (MA-ARDS) constitutes an excellent and relevant tool for this aim, since we already obtained clear preliminary data on glucocorticoid resistance in this model. Using state-of-the-art technologies, we aim to expand this concept to other AIMs, to investigate the impact of the resistance to AIMs on the development of immunopathologies and to define the immunological and biochemical mechanisms that govern the resistance. This project is therefore not only relevant for MA-ARDS, but will enhance our general knowledge on the regulation of inflammation.