RE: Universal study16 Aug 2024 22:05
someone with more knowledge than i will have to explain it gampy. (there are quite a few..) here's another mouse study from 2018 exploring the role of ifns in ards sepsis.
"recently, an open-label trial of systemic ifn-β improved 28-day survival in patients with ards (29). ifn-β is a type i ifn family member usually produced in response to viral infections and various pathogen-associated molecules (e.g., lps), and it exerts pleiotropic effects such as viral inhibition, tumor killing, and immune modulation (30, 31). ifn-β also stimulates expression of ecto-5′-nucleotidase (cd73) in cultured endothelial cells (32) and in human lung tissue explants (29), which is associated with increased adenosine production, improved endothelial barrier function, and reduced vascular leakage, suggesting that ifn-β may function to reduce pulmonary edema. in murine models of sepsis and endotoxin-induced shock, ifn-β improves survival, possibly by silent mating type information regulation 2 ****log 1–mediated suppression of exaggerated cytokine expression (33). thus, ifn-β holds promise as a disease-specific therapy for ards, but there is insufficient knowledge about its potential therapeutic benefits.
patients with severe peritoneal infection usually experience nosocomial infections with high mortality. lung innate immunity, including the bactericidal capacity of alveolar macrophages, is impaired and may be associated with susceptibility to nosocomial infections. potent immune-enhancing mediator ifn-β restores functional impairment of alveolar macrophages and may be a new therapeutic target for sepsis-related immune suppression.
https://www.ncbi.nlm.nih.gov/pmc/articles/pmc6835072/