BackgroundChronic rhinosinusitis (CRS) is a frequent disease with high social impact and multifactorial pathogenesis. Recently, single nucleotide polymorphisms within the TAS2R38 gene have been implicated as possible contributors to the complex gene-environment interactions in CRS.The purpose of this study was to confirm the proposed correlation between TAS2R38 genotype, CRS and related comorbidities.MethodsFifty-three CRS patients and 39 healthy individuals were genotyped at the TAS2R38 locus. CRS patients were treated by endoscopic sinus surgery and medical therapies and subdivided in CRS with nasal polyps (CRSwNPs) and CRS without nasal polyps (CRSsNPs). The effect of genotype on CRS and CRS-related comorbidities was assessed.ResultsThe distribution of the different genotypes at the TAS2R38 locus was not significantly different between CRS patients, either with or without nasal polyps, and controls. Besides, no association was found between the different genotypes at the TAS2R38 locus and CRS-related comorbidities.ConclusionsNo association was found between TAS2R38 alleles or genotypes and CRS, thus questioning its role in the pathogenesis of CRS.Electronic supplementary materialThe online version of this article (doi:10.1186/s12881-016-0321-3) contains supplementary material, which is available to authorized users.
The occurrence of DNA fragmentation in peripheral blood lymphocytes reflects a direct genotoxic effect of either alcohol or HBV and HCV and suggests that the same genotoxic effect may operate in the liver and contribute to hepatocarcinogenesis.
In the present study, the protective role of inulin against lipopolysaccharide (LPS)-induced oxidative stress was evaluated on human colonic mucosa using a proteomic approach. Human colonic mucosa and submucosa were sealed between two chambers, with the luminal side facing upwards and overlaid with Krebs (control), LPS or LPS+ inulin solution. The solutions on the submucosal side (undernatants) were collected following 30 min of mucosal exposure. iTRAQ based analysis was used to analyze the total soluble proteomes from human colonic mucosa and submucosa treated with different undernatants. Human colonic muscle strips were exposed to the undernatants to evaluate the response to acetylcholine. Inulin exposure was able to counteract, in human colonic mucosa, the LPS-dependent alteration of some proteins involved in the intestinal contraction (myosin light chain kinase (MLCK), myosin regulatory subunit (MYL)), to reduce the up-regulation of two proteins involved in the radical-mediated oxidative stress (the DNA-apurinic or apyrimidinic site) lyase APEX1 and the T-complex protein 1 subunit eta (CCT7) and to entail a higher level of some detoxification enzymes (the metallothionein-2 MT2A, the glutathione–S-transferase K GSTk, and two UDP- glucuronosyltransferases UGT2B4, UGT2B17). Inulin exposure was also able to prevent the LPS-dependent intestinal muscle strips contraction impairment and the mucosa glutathione level alterations. Exposure of colonic mucosa to inulin seems to prevent LPS-induced alteration in expression of some key proteins, which promote intestinal motility and inflammation, reducing the radical-mediated oxidative stress.
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