Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học Critical Care giúp cho các bạn có thêm kiến thức về ngành y học đề tài: Host immune response in sepsis due to ventilator-associated pneumonia: how is it different? | Available online http content 13 6 1009 Commentary Host immune response in sepsis due to ventilator-associated pneumonia how is it different Eirini Christaki Division of Infectious Diseases The Warren Alpert Medical School of Brown University The Miriam Hospital 164 Summit Avenue Providence RI 02906 USA Corresponding author Eirini Christaki Published 7 December 2009 Critical Care 2009 13 1009 doi cc8174 This article is online at http content 13 6 1009 2009 BioMed Central Ltd See related research by Pelekanou et al. http content 13 6 R172 Abstract Current evidence regarding potentially different host response mechanisms in sepsis according to the type of initiating infection is sporadic. It is possible that alterations in cell populations variations in effector molecules and the degree of apoptosis differ between sepsis caused by ventilator-associated pneumonia VAP and non-VAP sepsis. VAP is one of the most common infections and leading causes of sepsis in the intensive care unit and mortality remains high. A better understanding of the unique pathophysiologic features of VAP is needed in order to develop interventions that target those specific pathways. Ventilator-associated pneumonia VAP develops commonly in mechanically ventilated patients and is a major cause of morbidity and mortality in the intensive care unit. In a study published in this issue of Critical Care Pelekanou and colleagues 1 investigated the differences in innate and adaptive immune responses in 36 septic patients with VAP and 32 patients with sepsis due to other infections like pyelonephritis bacteremia intra-abdominal infection and community- and hospital-acquired pneumonia. There was evidence of a more pronounced immunoparalysis in patients with VAP than in those with other bacterial infections. This was supported by the decreased number of CD3 CD4 cells the increase in monocyte apoptosis and the lower release of .
