Sepsis articles from across Nature Portfolio

Chevrier and colleagues uncovered a hierarchical cytokine circuit arising from the pairwise effects of TNF with IL-18, IFN-γ or IL-1β, which explains the organism-wide response of the host to bacterial sepsis.

Vascular endothelial cadherin (VE-cadherin), endothelial cell-cell adhesive protein maintains blood vessel barrier integrity and vascular homeostasis. Here, the authors show that infectious bacterial toxin activates ubiquitin ligase CHFR which in turn degrades VEcadherin via ubiquitylation in endothelial cells to cause vascular injury.

The placenta nourishes the foetus and supports its development and growth. Our study now identifies the placenta as a potential route for foetal infection with Streptococcus agalactiae (group B Streptococcus), as indicated by an exaggerated in utero inflammatory response and poor perinatal outcome when group B Streptococcus is detected in the placenta.

Glycolysis provides building blocks for the proinflammatory activation of macrophages and simultaneously generates pyruvate. In this issue of Nature Metabolism, Ran et al. provide evidence that the transport of pyruvate to fuel the Krebs cycle in the mitochondria is not required in the inflammatory response.

A blood single-cell atlas of human sepsis identifies subsets of immune-suppressive neutrophils in people at high risk.