Persistent Activation of Sphingosine-1-Phosphate Receptor 1 by Phytosphingosine-3,4-Cyclic Phosphate Ameliorates Sepsis by Inhibiting Hyperinflammation and Vascular Hyperpermeability.

Sepsis is a life-threatening disease characterized by multiorgan dysfunction caused by an abnormal immune response to microbial infection. Sphingosine-1-phosphate (S1P) levels are significantly lower in patients with sepsis and are negatively correlated with the severity of sepsis. However, whether the S1P signaling pathway is a target for sepsis treatment remains unknown.

Interferon-β alleviates sepsis by SIRT1-mediated blockage of endothelial glycocalyx shedding.

Sepsis is a life-threatening multi-organ dysfunction with high mortality caused by the body's improper response to microbial infection. No new effective therapy has emerged that can adequately treat patients with sepsis. We previously demonstrated that interferon-β (IFN-β) protects against sepsis via sirtuin 1-(SIRT1)-mediated immunosuppression.

Changes in the phosphorylation of nucleotide metabolism‑associated proteins by leukemia inhibitory factor in mouse embryonic stem cells.

Leukemia inhibitory factor (LIF) is a stem cell growth factor that maintains self‑renewal of mouse embryonic stem cells (mESCs). LIF is a cytokine in the interleukin‑6 family and signals via the common receptor subunit gp130 and ligand‑specific LIF receptor. LIF causes heterodimerization of the LIF receptor and gp130, activating the Janus kinase/STAT and MAPK pathways, resulting in changes in protein phosphorylation.