Effects of dietary Phellinus linteus polysaccharides supplementation on productive performance, egg quality, antioxidant status, immune function, cecal microbiota, jejunal morphology, and metabolism in laying hens under lipopolysaccharide challenge.

Systematic pharmacology-guided analysis of the therapeutic mechanism of Sedum sarmentosum against chronic liver injury.

Acute inflammation is a complex biological response triggered by various invading agents provoking distinct immune pathways. As inter-strain variability in guinea pigs can influence inflammatory responses, ultimately affecting disease progression, understanding these strain-specific differences can improve the reliability and translational relevance of guinea pig models for studying acute inflammation. In this study, two guinea pig strains, Trik coloured and Dunkin-Hartley albino, were subjected to bacterial endotoxin lipopolysaccharide (LPS) to induce acute systemic inflammation. Specific metabolite alterations in the blood plasma and bronchoalveolar lavage fluid (BALF) were identified using hydrogen-1 nuclear magnetic resonance (¹H NMR) spectroscopy. Distinct differences in the metabolomic profiles in the blood plasma indicated significant inter-strain variability in circulating metabolites during LPS-induced acute inflammation, including those involved in amino acid transamination, ammonia transfer, and immune responses. Metabolomic analysis of BALF from guinea pigs with LPS-induced inflammation revealed decreased levels of specific metabolites. Moreover, changes in blood and BALF white blood cell counts and body weight were evaluated after LPS exposure. In BALF, LPS caused a slight, non-significant increase in total cell count and a significant neutrophil increase in the Dunkin-Hartley strain. In blood, Trik strain showed a significant increase in total count of cells and a significant neutrophil decrease. LPS induced weight loss in both strains, more pronounced in Trik. The study points out strain-specific metabolomic changes in guinea pig LPS model, highlighting the importance of strain selection in inflammation research. While descriptive, these preliminary findings provide a basis for future work to explore inflammatory mechanisms of LPS and improve translation to human disease.

Bifidobacterium supplementation ameliorates LPS-induced immune stress and intestinal barrier dysfunction in goslings.

Jagged1-Notch1/Foxo1 signaling crosstalk regulates TXNIP/NLRP3 inflammasome to alleviate lung inflammation.

Combined effects of incubation temperature and lipopolysaccharide exposure on immune response modulation in the quail gut.

Gallic acid attenuates LPS-induced hepatic injury via SIRT-1-dependent immunomodulation and anti-apoptotic mechanisms in rats.

Protective Effect of Docosahexaenoic Acid Supplementation during Pregnancy against Lipopolysaccharide-Induced Intrauterine Growth Restriction in Fetal Mice.

The connection between oral and systemic diseases is receiving increasing attention. Pulpitis is an infectious disease, and its potential impact on the systemic system deserves further investigation. A rat/mouse pulpitis model was utilized to explore the variations in bone morphogenetic protein 9 (BMP9) and lipopolysaccharide (LPS) concentrations within liver tissue and blood. Hepatic stellate cells were cultivated and subsequently stimulated with LPS. Histone H3K9 methylation and associated methyltransferase levels were quantified. G9a function was investigated by the G9a methyltransferase inhibitor UNC0642. In rats and mice with pulpitis, BMP9 expression initially declined in both the liver and blood, followed by a subsequent increase. This BMP9 trend in LPS-stimulated hepatic stellate cells mirrored the findings observed in vivo. Mechanistically, the involvement of H3K9 dimethylation and G9a methyltransferase in this process was elucidated. Treatment with UNC0642 successfully restored suppressed BMP9 levels. Chromatin immunoprecipitation assays further confirmed an increased enrichment of H3K9 dimethylation in the promoter region of the BMP9 gene following LPS stimulation of mouse hepatic stellate cells. These findings suggested that LPS in pulpitis might transiently influence the expression of BMP9 in liver tissues, and pulpitis might have potential effects on systemic tissues and organs. This study provides a proof-of-concept for targeting epigenetic pathways to mitigate the oral-systemic disease link, motivating future clinical trials in high-risk populations.

Weizmannia coagulans BC99 alleviates alcohol-induced oxidative stress and gut barrier dysfunction via modulation of butyrate metabolism: A randomized, double-blind, placebo-controlled trial.

Ferrostatin-1 attenuates sepsis-induced lung injury by inhibiting ferroptosis via activation of the SLC7A11/GSH/GPX4 signaling pathway.

Rab32-mediated macrophage apoptosis and apoptotic body release promote M1 polarization in ARDS via the Cxcl11/Ccl4/NF-κB pathway.

Hyperoside as a promising multi-target candidate for neovascular age-related macular degeneration. mechanisms involving Wnt/β-catenin signaling, oxidative stress, and inflammation suppression.

Citrus flavonoid-enriched milk protects against intestinal oxidative stress and barrier dysfunction in mice.

Withanolides from Physalis minima as potential anti-inflammatory agents: From isolation to in vitro and in vivo validation.

Integrative bioinformatics identifies NSCLC biomarkers associated with LPS metabolism and circadian disruption.

1-O-acetylbritannilactone alleviates high-fat diet-induced fatty liver by covalently targeting NLRP3.

The rabies glycoprotein C-terminal peptide attenuates LPS-induced synaptic dysfunction and cognitive impairment in male rats.

Small nucleolar RNA host gene 3 regulates sepsis-induced acute lung injury and inflammation by targeting microRNA-186-5p.

Yu Dan Tong Formula inhibits NLRP3 inflammasome activation by suppressing Ca²⁺ influx in treating cholestatic liver disease.