Alverdy John C, Krezalek Monika A
All authors: The Department of Surgery, University of Chicago, Pritzker School of Medicine, Chicago, IL.
Crit Care Med. 2017 Feb;45(2):337-347. doi: 10.1097/CCM.0000000000002172.
The definition of sepsis has been recently modified to accommodate emerging knowledge in the field, while at the same time being recognized as challenging, if not impossible, to define. Here, we seek to clarify the current understanding of sepsis as one that has been typically framed as a disorder of inflammation to one in which the competing interests of the microbiota, pathobiota, and host immune cells lead to loss of resilience and nonresolving organ dysfunction. Here, we challenge the existence of the idea of noninfectious sepsis given that critically ill humans never exist in a germ-free state. Finally, we propose a new vision of the pathophysiology of sepsis that includes the invariable loss of the host's microbiome with the emergence of a pathobiome consisting of both "healthcare-acquired and healthcare-adapted pathobiota." Under this framework, the critically ill patient is viewed as a host colonized by pathobiota dynamically expressing emergent properties which drive, and are driven by, a pathoadaptive immune response.
脓毒症的定义最近已被修改，以适应该领域新出现的知识，同时，即便不是无法定义，其定义也被认为具有挑战性。在此，我们试图阐明对脓毒症的当前理解，即脓毒症通常被视为一种炎症紊乱，而现在应理解为微生物群、致病生物群和宿主免疫细胞之间相互竞争的利益导致机体恢复力丧失和器官功能障碍持续存在。鉴于重症患者并非处于无菌状态，我们对非感染性脓毒症这一概念的存在提出质疑。最后，我们提出了脓毒症病理生理学的新观点：随着由“医疗保健获得性和医疗保健适应性致病生物群”组成的致病生物群的出现，宿主微生物群不可避免地丧失。在此框架下，重症患者被视为由致病生物群定植的宿主，这些致病生物群动态表达出一些新兴特性，这些特性驱动并受适应性免疫反应驱动。
