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LUTFIOGLU, MUGE/0000-0003-1499-5902 WOS: 000379914800006 PubMed: 26446985 Background and ObjectiveSmoking is an important risk factor for periodontal disease and effects the pathogenesis of the disease. This study evaluated the impact of smoking on gingival crevicular fluid interleukin-8 (IL-8) and lipoxin A(4) (LxA(4)) levels in patients with and without periodontal disease. Material and MethodsA total of 122 participants were grouped as follows: smokers with generalized aggressive periodontitis (S-GAgP, n = 15); smokers with chronic periodontitis (S-CP, n = 17); smokers with gingivitis (SG, n = 15); smokers classified as periodontally healthy (SH, n = 15); nonsmokers with generalized aggressive periodontitis (N-GAgP, n = 15); nonsmokers with chronic periodontitis (N-CP, n = 15); nonsmokers with gingivitis (NG, n = 15); and nonsmokers classified as periodontally healthy (NH, n = 15). Gingival index, plaque index, probing pocket depth and clinical attachment level were recorded. Gingival crevicular fluid IL-8 and LxA4 levels were analyzed by ELISA. ResultsGingival crevicular fluid IL-8 levels varied among groups, as follows: S-GAgP>S-CP>SG>SH and N-GAgP>N-CP>NG>NH. The gingival crevicular fluid IL-8 levels were significantly higher in the S-GAgP group compared with the N-GAgP group and in the S-CP group compared with the N-CP group (p < 0.05); differences between the SG and NG and the SH and NH groups were not statistically significant (p > 0.05). Gingival crevicular fluid LxA(4) levels also varied among groups, but in an inverse direction when compared with the IL-8 levels, as follows: S-GAgP 0.05). ConclusionThe study findings suggest that the observed increases in gingival crevicular fluid IL-8 levels and decreases in gingival crevicular fluid LxA(4) levels reflect changes in immune and inflammatory responses that occur as a result of smoking.

The G-protein coupled receptor formyl peptide receptor 2 (FPR2) integrates signals of multiple anti-inflammatory and anti-fibrotic mediators including lipoxin A4, resolvin D1, and annexin A1. Previ...

The effect of the eight lipoxin A4 analogues (I) and (II) on cytokines is evaluated with (Ic) and (IId) showing a significant reduction in the production of specific pro-inflammatory cytokines.

The active resolution of inflammation is recognized as offering new opportunities to generate novel anti-inflammatory agents. The emerging appreciation of the importance of active resolution in regulation of inflammation also creates an imperative to examine developing and existing agents for their potential to influence these pathways. This themed issue of the British Journal of Pharmacology contains papers that discuss the roles of annexin-1, lipoxins and related lipid products of fish oils as well as other mechanisms involved in active resolution and their receptor targets. This article is part of a themed issue on Mediators and Receptors in the Resolution of Inflammation. To view this issue visit http://www3.interscience.wiley.com/journal/121548564/issueyear?year=2009

The mechanism of action of aspirin (ASA) is related to cyclooxygenase (COX) inhibition, but additional actions cannot be excluded for their antiinflammatory properties and antithrombotic activity. In the current investigation, we examined the effects of ASA on COX and 5-lipoxygenase (5-LO) pathways and its impact on peroxisome proliferator-activated receptor alpha (PPARalpha) and cytokine-induced neutrophil chemoattractant-1 (CINC-1) levels in rat liver cells. In Kupffer cells, the liver resident macrophages, ASA switched eicosanoid biosynthesis from prostaglandin E2 (PGE2) to leukotriene B4 (LTB4) and 15-epi-lipoxin A4 (15-epi-LXA4) formation. In hepatocytes, ASA significantly inhibited PPARalpha protein expression and CINC-1 secretion, effects that were also observed in hepatocytes exposed to the selective PPARalpha agonist Wy-14643. In contrast, treatment of hepatocytes with PGE2 in association with LTB4 had no significant effect on PPARalpha but stimulated CINC-1 release. Interestingly, the endogenous antiinflammatory eicosanoids LXA4 and ASA-triggered 15-epi-LXA4, in addition to inhibiting macrophage 5-LO activity to a similar extent as PGE2, significantly reduced PPARalpha and CINC-1 levels in hepatocytes. Taken together and because arachidonic acid-derived products, PPARalpha levels, and CINC-1 secretion are involved in the extent and duration of an inflammatory response, these findings provide additional molecular mechanisms for the pharmacological properties of ASA.

A new facile route to (2E,4E)-dienals by a double formyl-olefination with arsonium salts has been developed. By this method and with other arsonium reagents in the key step some lipoxygenase metabolites of arachidonic acid, lipoxin A4 and B4 and leukotriene B4, have been synthesized.