Anti-F4/80 monoclonal antibody, clone CN9.2 [violetFluor™ 450]

Chronic periodontitis (CP) is a common oral disease that confers substantial systemic inflammatory and microbial burden and is a major cause of tooth loss. Here, we present the results of a genome-wide association study of CP that was carried out in a cohort of 4504 European Americans (EA) participating in the Atherosclerosis Risk in Communities (ARIC) Study (mean ageu62 years, moderate CPu43 and severe CPu17). We detected no genome-wide significant association signals for CP; however, we found suggestive evidence of association (P 5 10(6)) for six loci, including NIN, NPY, WNT5A for severe CP and NCR2, EMR1, 10p15 for moderate CP. Three of these loci had concordant effect size and direction in an independent sample of 656 adult EA participants of the Health, Aging, and Body Composition (Health ABC) Study. Meta-analysis pooled estimates were severe CP (n 958 versus health: n 1909)uNPY, rs2521634 [G]: odds ratio [OR 1.49 (95 confidence interval (CI 1.281.73, P 3.5 10(7)))]; moderate CP (n 2293)uNCR2, rs7762544 [G]: OR 1.40 (95 CI 1.241.59, P 7.5 10(8)), EMR1, rs3826782 [A]: OR 2.01 (95 CI 1.522.65, P 8.2 10(7)). Canonical pathway analysis indicated significant enrichment of nervous system signaling, cellular immune response and cytokine signaling pathways. A significant interaction of NUAK1 (rs11112872, interaction P 2.9 10(9)) with smoking in ARIC was not replicated in Health ABC, although estimates of heritable variance in severe CP explained by all single nucleotide polymorphisms increased from 18 to 52 with the inclusion of a genome-wide interaction term with smoking. These genome-wide association results provide information on multiple candidate regions and pathways for interrogation in future genetic studies of CP.

Chronic low-grade inflammation in obesity is characterized by macrophage accumulation in white adipose tissue (WAT) and abnormal cytokine production. We tested the hypothesis that grape-seed procyanidin extract (PE), with known anti-inflammatory and antioxidant effects, would improve local and systemic inflammation in diet-induced obesity rats. First, we analyzed the preventive effects of procyanidins (30 mg/kg per day) on rats fed a 60% kcal fat diet for 19 weeks. Second, we induced cafeteria diet obesity for 13 weeks to investigate the corrective effects of two PE doses (25 and 50 mg/kg per day) for 10 and 30 days. In the preventive model, PE group had reduced not only body weight but also plasmatic systemic markers of inflammation tumor necrosis factor-alpha (TNF-alpha) and C-reactive protein (CRP). The PE preventive treatment significantly showed an increased adiponectin expression and decreased INF-alpha, interleukin-6 and CRP expression in mesenteric WAT and muscle TNF-alpha. A reduced NF-kappa B activity in liver is also observed which can be related to low expression rates of hepatic inflammatory markers found in PE group. Finally, PE dietary supplementation is linked to a reduced expression of Emr1 (specific marker of macrophage F4/80), which suggests a reduced macrophage infiltration of WAT. In the corrective model, however, only the high dose of PE reduced CRP plasma levels in the short treatment without changes in plasmatic INF-alpha. In conclusion, orally ingested PE helps preventing imbalanced obesity cytokine pattern, but its corrective effects need to be further investigated. The dietary regular intake of food or drinks containing procyanidins might help prevent low-grade inflammatory-related diseases. (C) 2011 Elsevier Inc. All rights reserved.