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: Direct effects of modest hyperglycaemia on susceptibility to infection in the critically ill patient. | Available online http content 12 6 433 Letter Direct effects of modest hyperglycaemia on susceptibility to infection in the critically ill patient Matt P Wise Anton G Saayman and Paul J Frost Adult Critical Care University of Hospital of Wales Heath Park Cardiff CF14 4XW UK Corresponding author Matt P Wise mattwise@ Published 5 November 2008 This article is online at http content 12 6 433 2008 BioMed Central Ltd Critical Care 2008 12 433 doi cc7089 See related research by Otto et al. http content 12 4 R107 In their recent study Otto and colleagues suggested that the adverse effects of hyperglycaemia on immune function may be mediated by hyperosmotic stress 1 . In granulocytes both oxidative burst and phagocytosis were suppressed by hyperosmolar stress with mannitol but no significant effect was observed on cytokine release from peripheral blood mononuclear cells 1 . The concentration of glucose and mannitol used in these experiments 500 mg dl or l however is rarely encountered in critically ill patients - and then only transiently. One may question how relevant this mechanism is when it appears that modest levels of hyperglycaemia mmol l have deleterious effects in this population 2 . Modest hyperglycaemia has been demonstrated to directly perturbate immune function by more than one mechanism. Macropinocytosis by macrophages involves nonspecific sampling of pathogens in extracellular fluid which are then directed towards antigen processing with subsequent presentation of microbial peptides to T cells linking innate and adaptive immunity. Macropinocytosis is reduced in a dosedependent manner by glucose but not by mannitol. Increasing glucose from to mmol l inhibited macropinocytosis by 55 3 . Surfactant proteins A and D and mannose-binding lectin are important host defence molecules collectins which bind pathogens augment opsonisation phagocytosis and killing by macrophages and .
