TAILIEUCHUNG - Nature reviews Immunology voLume 11

Statins inhibit cholesterol synthesis and are prescribed to those at high risk of developing cardiovascular disease. The widespread use of these drugs has promoted interest in their other effects: this study shows that statins affect phagocyte functions. Pre-treatment with statins increased the capacity of human neutrophils and macrophages to kill various bacteria in vitro, but paradoxically, statins decreased the ability of neutrophils to phagocytose Staphylococcus aureus or induce the oxidative burst | RESEARCH HIGHLIGHTS IN BRIEF 2 INNATE IMMUNITY Statins enhance formation of phagocyte extracellular traps Chow O. A. et al. Cell Host Microbe 8 445-454 2010 Statins inhibit cholesterol synthesis and are prescribed to those at high risk of developing cardiovascular disease. The widespread use of these drugs has promoted interest in their other effects this study shows that statins affect phagocyte functions. Pre-treatment with statins increased the capacity of human neutrophils and macrophages to kill various bacteria in vitro but paradoxically statins decreased the ability of neutrophils to phagocytose Staphylococcus aureus or induce the oxidative burst. Instead statins promoted microbial killing by inducing phagocyte production of extracellular traps mesh-like structures composed of nuclear DNA histones and antimicrobial peptides . In a model of S. aureus-induced pneumonia pre-treating mice with statins decreased bacterial loads and pathology in the lungs and this was associated with increased formation of extracellular traps. Patients with pneumonia or sepsis have better survival rates if they are receiving statin therapy this study may explain these findings. INFLAMMATION A role for mitochondria in NLRP3 inflammasome activation Zhou R. et al. Nature 1 Dec 2010 doi nature09665 The NLRP3 NOD- LRR- and pyrin domain-containing 3 inflammasome is activated in response to pathogens or damaged cells and promotes the maturation of inflammatory cytokines such as interleukin-1p IL-1p . It is currently unclear how diverse danger signals activate the NLRP3 inflammasome but one model proposes that the generation of reactive oxygen species ROS is involved. This study shows that stressed mitochondria are a rich source of ROS that trigger inflammasome activation. Inhibition of mitochondrial function led to ROS release and subsequent IL-1p induction in wild-type but not NLRP3-deficient macrophages. Healthy cells remove ROS-generating mitochondria through mitophagy a .

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