Anti-IL6 monoclonal antibody, clone CC310

We evaluated the effect of gut bacterial metabolites of polyunsaturated fatty acids on inflammation and found that 10-oxo-cis-6,trans-11-octadecadienoic acid (gamma KetoC) strikingly suppressed LPS-induced IL-6 release from bone marrow-derived macrophages (BMMs), which was accompanied by reduced mRNA expression of Il6, TNF, and Il1b. gamma KetoC decreased the cAMP concentration in BMMs, suggesting that gamma KetoC stimulated G protein-coupled receptors. A Gq agonist significantly suppressed LPS-induced IL-6 expression in BMMs, whereas a Gi inhibitor partially abrogated gamma KetoC-mediated IL-6 suppression. Cytosolic Ca2+ was markedly increased by gamma KetoC, which was partly but not fully abrogated by an ion channel inhibitor. Taken together, these data suggest that gamma KetoC suppresses inflammatory cytokine expression in macrophages primarily through Gq and partially through Gi. gamma KetoC suppressed osteoclast development and IL-6 expression in synovial fibroblasts from rheumatoid arthritis (RA) patients, suggesting the beneficial effect of gamma KetoC on the prevention or treatment of RA. (c) 2020 Elsevier Inc. All rights reserved.

Glaesserella parasuis(G. parasuis) causes porcine vascular inflammation and damage. Baicalin is reported to have antioxidant and anti-inflammatory functions. However, whether baicalin protects piglets againstG. parasuischallenge and the potential protective mechanism have not been investigated. Therefore, in this study, we comprehensively examined the protective efficacy of baicalin in piglets challenged withG. parasuisand the possible protective mechanism. Our results show that baicalin attenuated the release of the inflammation-related cytokines interleukin (IL) 1 beta, IL6, IL8, IL10, and tumour necrosis factor alpha (TNF-alpha) and reduced high mobility group box 1 (HMGB1) production and cell apoptosis in piglets infected withG. parasuis. Baicalin also inhibited the activation of the mitogen-activated protein kinase (MAPK) signalling pathway and protected piglets againstG. parasuischallenge. Taken together, our data suggest that baicalin could protect piglets fromG. parasuisby reducing HMGB1 release, attenuating cell apoptosis, and inhibiting MAPK signalling activation, thereby alleviating the inflammatory response induced by the bacteria. Our results suggest that baicalin has utility as a novel therapeutic drug to controlG. parasuisinfection.