DHA suppressesPrevotella intermedialipopolysaccharide-induced production of proinflammatory mediators in murine macrophages

Abstract

Several reports have indicated that dietary intake of DHA is associated with lower prevalence of periodontitis. In the present study, we investigated the effect of DHA on the production of proinflammatory mediators in murine macrophage-like RAW264.7 cells stimulated with lipopolysaccharide (LPS) isolated from Prevotella intermedia, a pathogen implicated in inflammatory periodontal disease, and its mechanisms of action. LPS was isolated from lyophilised P. intermedia ATCC 25 611 cells using the standard hot-phenol -water protocol. Culture supernatants were collected and assayed for NO, IL-1b and IL-6. Real-time PCR analysis was carried out to detect the expression of inducible NO synthase (iNOS), IL-1b, IL-6 and haeme oxygenase-1 (HO-1) mRNA. Immunoblot analysis was carried out to quantify the expression of iNOS and HO-1 protein and concentrations of signalling proteins. DNA-binding activities of NF-kB subunits were determined using an ELISA-based assay kit. DHA significantly attenuated the production of NO, IL-1b and IL-6 at both gene transcription and translation levels in P. intermedia LPS-activated RAW264.7 cells. DHA induced the expression of HO-1 in cells treated with P. intermedia LPS. Selective inhibition of HO-1 activity by tin protoporphyrin IX significantly mitigated the inhibitory effects of DHA on LPS-induced NO production. DHA significantly attenuated the phosphorylation of c-Jun N-terminal kinase induced by LPS. In addition, DHA suppressed the transcriptional activity of NF-kB by regulating the nuclear translocation and DNA-binding activity of NF-kB p50 subunit and inhibited the phosphorylation of signal transducer and activator of transcription 1. Further in vivo studies are needed to better evaluate the potential of DHA in humans as a therapeutic agent to treat periodontal disease.

Social Influences on Prevotella and the Gut Microbiome of Young Monkeys

“…The clustering of gut microbiota profiles by peer group is consistent with our first experiment showing that microbiotic dissimilarity within a group decreased by two weeks after group formation. Microbial convergence within a group would also be in keeping with reports of similar microbial profiles among members of the same household, for farm animals in a shared pen, and even between children and their pet companion animals (57–61). Cohousing and cohabitation effects on the microbiota have also been noted in other rodent and primate studies (7–9).…”

Overexpression of Receptor for Advanced Glycation End Products and High-Mobility Group Box 1 in Human Dental Pulp Inflammation

“…In addition, P. intermedia LPS has unique chemical and immunobiological characteristics considerably different from those of the classical LPSs from Escherichia coli and Salmonella species [41–43]. Previous studies have shown that P. intermedia LPS induced several mediators of inflammation in human dental pulp cells [8, 9], murine macrophages [44], and bone cells [45] and demonstrated inflammatory responses in mice [46]. Our data show for the first time that LPS from P. intermedia would be able to upregulate the danger signals HMGB1 and RAGE in human dental pulp inflammation.…”

Impact of physical exercise on visceral adipose tissue fatty acid profile and inflammation in response to a high-fat diet regimen

“…Therefore, this inflammatory state triggers the secretion of macrophage chemoattractant protein (MCP)-1 by macrophages, which can either sustain a macrophage-like phenotype in undifferentiated precursor cells or diminish the ability of adipocytes to further expand and store lipids, thus supporting a deleterious "vicious cycle" (7,8). Some recent studies reported that specific FA, such as saturated fatty acids (SFA) (9,10), monounsaturated fatty acids (11) and n6-polyunsaturated fatty acids (PUFA) (12) are involved in the pathophysiology of inflammation during obesity (1,2,13,14). In fact, a fat diet rich in SFA likely enhance circulating biomarkers of (pro) inflammation in health individuals (10), and in vitro studies showed that macrophages exposed to SFA increased pro-inflammatory gene expression and cytokine secretion, such as TNF-α and IL-6, and the chemokine CXCL1/KC (9).…”

“…Some recent studies reported that specific FA, such as saturated fatty acids (SFA) (9,10), monounsaturated fatty acids (11) and n6-polyunsaturated fatty acids (PUFA) (12) are involved in the pathophysiology of inflammation during obesity (1,2,13,14). In fact, a fat diet rich in SFA likely enhance circulating biomarkers of (pro) inflammation in health individuals (10), and in vitro studies showed that macrophages exposed to SFA increased pro-inflammatory gene expression and cytokine secretion, such as TNF-α and IL-6, and the chemokine CXCL1/KC (9). A MUFA-enriched high-fat diet (HFD) reverted inflammation-mediated insulin resistance and adipose tissue dysfunction when compared with SFA-fed mice (14).…”