%0 Journal Article
%T SAMP-ening down sepsis
%A Alison Coady
%A Victor Nizet
%J SCIE-indexed Journal
%D 2016
%R 10.21037/atm.2016.11.31
%X The inflammatory response is a critical component of innate immunity and required for controlling infection, clearing cellular damage, and initiating tissue repair. While this response is usually self-limiting and tightly controlled, inflammation can sometimes be aberrantly activated and prove injurious to host tissues, leading to acute or chronic disease pathologies. Perhaps the most dramatic of such pathologies is sepsis, a dysregulated inflammatory response to infection that can precipitate multiple organ system failure. Sepsis is a leading cause of mortality in hospital ICUs (1), and a recent global estimate attributed over 5 million deaths annually to this condition (2). Current treatment for sepsis remains mostly supportive, focusing on controlling infection and preventing organ failure. Thus, there remains a critical need for novel sepsis therapeutics. Multiple immune modulatory therapeutic strategies have been attempted, but the complexity of the disease, the diversity of underlying causes, and the heterogeneity of patient responses has yielded disappointing results in clinical trials (3). In a recent edition of Science Translational Medicine, Spence et al. (4) approached the treatment of sepsis-induced inflammation via a novel approach. Rather than attempting to neutralize a single molecular or cellular driver of inflammation, they stimulated a host Siglec receptor, a key anti-inflammatory regulator, using a nanoparticle decorated with the Siglec¡¯s natural ligand, sialic acid, a sugar that exemplifies a ¡°self-associated molecular pattern¡± (SAMP)
%U http://atm.amegroups.com/article/view/12994/html