Opal S M, Cohen J
Brown University School of Medicine, Povidence, RI, USA.
Crit Care Med. 1999 Aug;27(8):1608-16. doi: 10.1097/00003246-199908000-00039.
To review the basic differences between gram-positive and gram-negative sepsis and to assess the effect of these differences on current and future therapeutic strategies for sepsis.
Literature review of the past 30 yrs of laboratory and clinical reports that analyze the microbial aspects of sepsis and the immunologic response to systemic infection.
The increasing prevalence of sepsis from gram-positive bacterial pathogens necessitates reevaluation of many of the basic assumptions about the molecular pathogenesis of septic shock. It has been assumed that the initiation of the systemic inflammatory response with activation of the proinflammatory cytokine networks and other mediators results in a similar pathophysiologic process, regardless of the causative microbic pathogen. Yet, there is increasing experimental evidence that fundamental differences exist in the host response to gram-positive bacterial pathogens compared with the host response to gram-negative organisms. Systemic immune activation during sepsis may promote the clearance of the microbic pathogen; however, generalized inflammation also contributes to the pathogenesis of septic shock. The balance between these beneficial and deleterious effects may differ between gram-positive and gram-negative pathogens.
Results of antimediator therapies in clinical trials in septic shock are inconclusive but suggest that the response may differ, depending on the type of microbic pathogen. The immune-mediated pathophysiologic mechanisms that underlie gram-positive sepsis and the potential interactions between the infecting microorganism and efficacy of anticytokine therapies require further investigation. Treatment strategies that explain the causative organism may be necessary for optimal use of immunoadjuvants in the future.
回顾革兰氏阳性菌败血症和革兰氏阴性菌败血症之间的基本差异，并评估这些差异对当前及未来败血症治疗策略的影响。
对过去30年的实验室和临床报告进行文献综述，这些报告分析了败血症的微生物学方面以及对全身感染的免疫反应。
革兰氏阳性菌病原体引起的败血症患病率不断上升，这就需要重新评估许多关于感染性休克分子发病机制的基本假设。一直以来人们认为，无论致病微生物病原体是什么，促炎细胞因子网络和其他介质的激活引发全身炎症反应，都会导致相似的病理生理过程。然而，越来越多的实验证据表明，与宿主对革兰氏阴性菌的反应相比，宿主对革兰氏阳性菌病原体的反应存在根本差异。败血症期间的全身免疫激活可能促进微生物病原体的清除；然而，全身性炎症也会导致感染性休克的发病。革兰氏阳性菌和革兰氏阴性菌病原体在这些有益和有害作用之间的平衡可能有所不同。
抗介质疗法在感染性休克临床试验中的结果尚无定论，但表明反应可能因微生物病原体类型而异。革兰氏阳性菌败血症背后的免疫介导病理生理机制以及感染微生物与抗细胞因子疗法疗效之间的潜在相互作用需要进一步研究。为了未来最佳地使用免疫佐剂，可能需要针对病原体的治疗策略。
