[Host immunosuppression in pathogenesis of sepsis and its clinical implication].
The excessive inflammatory response accompanied by a dramatic paralysis of cell-mediated immunity following severe trauma, shock and burns appears to be responsible for the increased susceptibility to subsequent sepsis. The mechanism of immunodepression is quite complicated, and it is clearly related to the primary injury or disease and also the treatment. Many studies have been done to elucidate essential processes involved in host innate antimicrobial action activities, including activation of the immune response and also its down-regulation, as well as the mechanisms of pharmacologic immune suppression. Presently, it is recognized that abnormal activation of the innate immune response often leads to macrophage deactivation, loss of antigen presentation capacity, T-cell anergy, and the rapid apoptotic loss of lymphoid tissues, which all contribute to the development of sepsis. Data are accumulating to suggest that restoration of immune function is necessary for the recovery from sepsis and subsequent multiple organ dysfunction syndrome (MODS). A better understanding of the activated innate immunity and its physiological response will help to develop new therapeutical approaches aiming at modulating the immune response in conditions such as sepsis.
Yao
Yong-ming
YM
Burns Institute, the First Affiliated Hospital of General Hospital of PLA, Beijing 100037, China.
D000917:Antibody Formation / Q000276:immunology; D003713:Dendritic Cells / Q000276:immunology; D006801:Humans; D007113:Immunity, Innate / Q000276:immunology*; D008264:Macrophages / Q000276:immunology; D009504:Neutrophils / Q000276:immunology; D018805:Sepsis / Q000276:immunology*; D013601:T-Lymphocytes / Q000276:immunology