[The role of extracorporeal removal of CO2 (ECCO2R) in the management of respiratory diseases]. / Place de l'épuration extracorporelle de CO2 (ECCO2R) dans la prise en charge des pathologies respiratoires.

INTRODUCTION: The aim of extracorporeal removal of CO2 (ECCO2R) is to ensure the removal of CO2 without any significant effect on oxygenation. ECCO2R makes use of low to moderate extracorporeal blood flow rates, whereas extracorporeal membrane oxygenation (ECMO) requires high blood flows. STATE OF THE ART: For each ECCO2R device it is important to consider not only performance in terms of CO2 removal, but also cost and safety, including the incidence of hemolysis and of hemorrhagic and thrombotic complications. In addition, it is possible that the benefits of such techniques may extend beyond simple removal of CO2. There have been preliminary reports of benefits in terms of reduced respiratory muscle workload. Mobilization of endothelial progenitor cells could also occur, in analogy to the data reported with ECMO, with a potential benefit in term of pulmonary repair. The most convincing clinical experience has been reported in the context of the acute respiratory distress syndrome (ARDS) and severe acute exacerbations of chronic obstructive pulmonary disease (COPD), especially in patients at high risk of failure of non-invasive ventilation. PERSPECTIVES: Preliminary results prompt the initiation of randomized controlled trials in these two main indications. Finally, the development of these technologies opens new perspectives in terms of long-term ventilatory support.

Microparticles and infectious diseases.

Membrane shedding with microvesicle (MV) release after membrane budding due to cell stimulation is a highly conserved intercellular interplay. MV can be released by micro-organisms or by host cells in the course of infectious diseases. Host MVs are divided according to cell compartment origin in microparticles (MPs) from plasma membrane and exosomes from intracellular membranes. MPs are cell fragments resulting from plasma membrane reorganization characterized by phosphatidylserine (PhtdSer) content and parental cell antigens on membrane. The role of MPs in physiology and pathophysiology is not yet well elucidated; they are a pool of bioactive molecules able to transmit a pro-inflammatory message to neighboring or target cells. The first acknowledged function of MP was the dissemination of a procoagulant potential via PhtdSer and it is now obvious than MPs bear tissue factor (TF). Such MPs have been implicated in the coagulation disorders observed during sepsis and septic shock. MPs have been implicated in the regulation of vascular tone and cardiac dysfunction in experimental sepsis. Beside a non-specific role, pathogens such as Neisseria meningitidis and Ebola Virus can specifically activate blood coagulation after TF-bearing MPs release in the bloodstream with disseminated intravascular coagulopathy and Purpura fulminans. The role of MPs in host-pathogen interactions is also fundamental in Chagas disease, where MPs could allow immune evasion by inhibiting C3 convertase. During cerebral malaria, MPs play a complex role facilitating the activation of brain endothelium that contributes to amplify vascular obstruction by parasitized erythrocytes. Phagocytosis of HIV induced MPs expressing PhtdSer by monocytes/macrophages results in cellular infection and non-inflammatory response via up-regulation of TGF-ß.