Pharmacological inhibition of RORγ activity reduced plasma IL-1β as well as IL-1β production by peritoneal macrophages in a model of LPS-induced sepsis.
IL-1β best predicted sepsis, with an area under the receiver operating characteristic (AUROC) of 0.71 (95% CI: 0.57-0.85); a combined biomarker-clinical characteristics model improved prediction (AUROC of 0.77, 95% CI: 0.67-0.85).
The potential significance of IL-1 members in sepsis will also be explored, together with the clinical implications for treating this dangerous condition.
In order to evaluate, if Lactobacillus rhamnosus GG (LGG) treatment in septic rats will protect against liver injury, this study used 20-22-week-old Sprague-Dawley rats which were subjected to cecal ligation and puncture to establish sepsis model and examine mRNA and protein levels of IL-1β, NLRP3, IL-6, TNF-a, VEGF, MCP1, NF-kB and HIF-1α in the liver via real-time PCR, Elisa and Western blot.
Pharmacological inhibition of de novo serine synthesis in vivo decreased LPS induction of IL-1β levels and improved survival in an LPS-driven model of sepsis in mice.
Methane suppressed the expression of the toll-like receptor 4/nuclear factor-kappa B (NF-κB) signaling pathway and stimulated the expression of peroxisome proliferator-activated receptor-γ (PPAR-γ) during sepsis, which inhibited the activation of NF-κB and decreased the level of inflammatory cytokines, such as tumor necrosis factor-α, interleukin-6, and interleukin-1β.
Several serum-based biomarkers such as C-reactive protein, lactate, presepsin, and cytokines, such as interleukin-1 (IL-1), and IL-6 have been evaluated as early indicators of sepsis but none have been proven sensitive and/or specific enough to make a definitive diagnosis.
Here, results showed that pretreatment with rapamycin reduced the pyroptosis of peritoneal macrophages stimulated by cecal contents and the release of inflammatory factors such as interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α); In septic mice, rapamycin treatment decreased the activation of inflammasome in lung, and alleviated the pathological injuries in lung, liver and spleen tissues during acute stage of sepsis.
The results of RT-qPCR demonstrated that the expression of miR-146a, TNF-α, IL-1α and IL-1β in the sepsis model group were upregulated compared with the control group.
<i>Usp19<sup>-/-</sup></i> mice produced higher levels of inflammatory cytokines and were more susceptible to TNF-α- and IL-1β-triggered septicemia death compared with their wild-type littermates.
Macrophages play an important role in the early stage of sepsis as they are tasked with eliminating invading microbes and also attracting other immune cells by the release of proinflammatory cytokines such as interleukin-1β, interleukin-6, and tumor necrosis factor-α.
The NLR family pyrin domain-containing 3 (NLRP3) inflammasome is a multimeric protein complex that mediates maturation of the cytokines IL-1β and IL-18 as well as release of the proinflammatory protein high-mobility group box 1 (HMGB1) and contributes to several inflammatory diseases, including sepsis, gout, and type 2 diabetes.
Circulating concentrations of CRP, PCT, interleukin (IL)-10 and IL-1 receptor antagonist (IL-1Ra) were significantly higher in patients with sepsis, with IL-10 identified as the best biomarker in differentiating sepsis from SIRS.
A correlation analysis showed that the levels of serum IL-37 and IL-1β were positively correlated.The level of IL-37 observed in sepsis was found to correlate with the severity of the inflammatory reaction.
Plasma interleukin-1 beta may influence sepsis mortality, yet recombinant human interleukin-1 receptor antagonist did not reduce mortality in randomized trials.
In our study, we found that AA decreased levels of interleukin-1β (IL-1β), IL-6, alanine aminotransferase and blood urea nitrogen in serum; attenuated liver, lung and kidney damage; and improved the survival among mice with experimental sepsis.
In human THP-1 cells, anti-IL-31/anti-IL-31 receptor (R) neutralizing antibody enhanced NLRP3 expression as well as IL-1β activation, suggesting a role of the IL-31-IL-31R-NLRP3-IL-1β signaling axis in the physiological status of sepsis.
In a sepsis model, pretreatment with FSB inhibited the LPS-stimulated mRNA and protein levels of proinflammatory mediators, such as, iNOS, COX-2, TNF-α, IL-6 and IL-1β in plasma and liver.
After IMD<sub>1-53</sub> treatment, inflammation caused by sepsis in vivo was greatly reduced, as shown by the downregulation of apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC), nucleotide-binding domain and leucine-rich repeat containing family, pyrin containing 3 (NLRP3), pro-IL-1β, caspase 1, and nuclear translocation of nuclear factor-κB (NF-kB) protein levels.