Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học quốc tế cung cấp cho các bạn kiến thức về ngành y đề tài: Understanding immune dysfunctions in sepsis patients. | López-Collazo et al. Critical Care 2010 14 435 http content 14 4 435 CRITICAL CARE LETTER L_ Understanding immune dysfunctions in sepsis patients Eduardo Lopez-Collazo1 Vanesa Gomez-Pina1 and Francisco Arnalich2 See related research by Gogos etal. http content W3 R96 We read with interest the article by Gogos and colleagues in a previous issue of Critical Care reporting that there are major differences in the early status of the innate and adaptative immune responses between sepsis and severe sepsis shock in relation to the underlying type of infection 1 . In patients with acute pyelonephritis and intraabdominal infection expression of HLA-DR on monocytes was significantly decreased among patients with severe sepsis shock compared with among patients only suffering sepsis. This difference was related to an unfavourable outcome in patients with acute pyelonephritis. The authors considered the decrease of CD14 HLA-DR co-expression to be an index of immunoparalysis and bad prognosis 1 . An altered expression of HLA-DR on the monocyte surface however is not synonymous with a global downregulation of cellular reactivity. The term cellular reprogramming thus appears the most appropriate to define the events occurring among circulating monocytes and other immune cells during severe sepsis shock 2 . In addition a growing set of evidence undoubtedly indicates that despite the Toll-like receptor IL-1 receptor-associated kinase NF-KB pathway being blocked other alternative signals are active simultaneously in septic patients 3-5 . Recently we analysed a cohort of 17 patients who met the diagnostic criteria for sepsis 6 see Figure 1 overleaf . Our findings demonstrated that these patients showed reduced responsiveness to a lipopolysaccharide challenge which is called endotoxin tolerance but their monocytes were not paralysed. As Figure 1a to 1f shows despite an evident downregulation of TNFa production after ex vivo lipopolysaccharide challenge .
