Medical Intensive Care Unit, NHC - Strasbourg University Hospital, Strasbourg, France.
EA 7293 FMTS, University of Strasbourg, Strasbourg, France.
Shock. 2018 Apr;49(4):371-384. doi: 10.1097/SHK.0000000000000980.
In addition to their well-known role as the cellular mediators of immunity, key other roles have been identified for neutrophils during septic shock. Importantly, neutrophils indeed play a critical role in the recently described immunothrombosis concept and in septic shock-induced coagulopathy. Septic shock is one of the most severe forms of infection, characterized by an inadequate host response to the pathogenic organism. This host response involves numerous defense mechanisms with an intense cellular activation, including neutrophil activation. Neutrophils are key cells of innate immunity through complex interactions with vascular cells and their activation may participate in systemic tissue damages. Their activation also leads to the emission of neutrophil extracellular traps, which take part in both pathogen circumscription and phagocytosis, but also in coagulation activation. Neutrophils thus stand at the interface between hemostasis and immunity, called immunothrombosis.The present review will develop a cellular approach of septic shock pathophysiology focusing on neutrophils as key players of septic shock-induced vascular cell dysfunction and of the host response, associating immunity and hemostasis. We will therefore first develop the role of neutrophils in the interplay between innate and adaptive immunity, and will then highlight recent advances in our understanding of immunothrombosis septic shock-induced coagulopathy.
除了作为免疫细胞的众所周知的作用外，中性粒细胞在感染性休克中还具有其他关键作用。重要的是，中性粒细胞确实在最近描述的免疫血栓形成概念和感染性休克引起的凝血功能障碍中发挥了关键作用。感染性休克是最严重的感染形式之一，其特征是宿主对病原体的反应不足。这种宿主反应涉及多种防御机制，包括强烈的细胞激活，包括中性粒细胞的激活。中性粒细胞通过与血管细胞的复杂相互作用成为先天免疫的关键细胞，其激活可能参与全身组织损伤。它们的激活还导致中性粒细胞细胞外陷阱的释放，这既参与病原体的局限和吞噬作用，也参与凝血激活。因此，中性粒细胞处于止血和免疫之间的界面，称为免疫血栓形成。本综述将从细胞角度探讨感染性休克的病理生理学，重点关注中性粒细胞作为感染性休克引起的血管细胞功能障碍和宿主反应的关键参与者，将免疫和止血联系起来。因此，我们将首先探讨中性粒细胞在先天免疫和适应性免疫相互作用中的作用，然后强调我们对感染性休克诱导的免疫血栓形成性凝血功能障碍的理解的最新进展。
