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IntroductionFollistatin-like protein 1 (FSTL1) is a proinflammation mediator implicated in arthritis in rodent animal models. The present study is aimed at assessing FSTL1 levels in systemic autoimmune diseases and correlating them with disease activity in patients with rheumatoid arthritis (RA).MethodsSerum FSTL1 levels from 487 patients with systemic autoimmune diseases and 69 healthy individuals were measured by enzyme-linked immunosorbent assay (ELISA). FSTL1 expression in synovial fluid (SF) and synovial tissues (STs) was determined by ELISA, immunohistochemistry, real-time polymerase chain reaction (RT-PCR) and western blot analysis in RA patients and trauma controls. FSTL1 levels in fibroblast-like synoviocytes (FLSs) from RA patients were determined by real-time PCR and western blot analysis.ResultsSerum FSTL1 levels were significantly elevated in patients with RA, ulcerative colitis, systemic lupus erythematosus, Sjögren's syndrome (SS), systemic sclerosis and polymyositis/dermatomyositis. Serum FSTL1 levels in the RA and secondary SS patients were substantially higher than those in other patients. Serum FSTL1 levels were increased in early RA, rheumatoid factor (RF)- and anti-cyclic citrullinated peptide antibody (ACPA)-negative patients compared to healthy controls. Moreover, serum FSTL1 concentrations were significantly higher in long-standing RA patients than in early RA patients and in the RF- and ACPA-positive RA patients than in RF- and ACPA-negative RA patients. Elevated FSTL1 levels in the STs and SF of RA patients were also observed. FSTL1 levels in serum were markedly higher than those in SF in RA patients. The strongest FSTL1 staining was detected in the cytoplasm of synovial and capillary endothelial cells from RA synovium. Furthermore, FSTL1 was induced in FLSs by inflammatory mediators. Importantly, serum FSTL1 levels were correlated with several important biologic and clinical markers of disease activity, including erythrocyte sedimentation rate, C-reactive protein, RF, ACPA, swollen joint count, patient global visual analogue scale score and Disease Activity Score 28 in the adult RA patient population. Notably, serum FSTL1 levels were significantly diminished following successful treatment and clinical improvement.ConclusionsElevated FSTL1 levels reflect not only joint diseases but also inflammation and tissue degradation in systemic autoimmune diseases. Serum FSTL1 levels may thus serve as a serological inflammatory marker of disease activity in RA patients.

Introduction Magnetic sphincter augmentation (MSA) results in less severe side effects compared with Nissen fundoplication, but dysphagia remains the most common side effect reported by patients after MSA. This study aimed to characterize and review the management of postoperative dysphagia and identify the preoperative factors that predict persistent dysphagia after MSA. Material and Methods This is a retrospective review of prospectively collected data of patients who underwent MSA between 2013 and 2018. Preoperative objective evaluation included upper endoscopy, esophagram, high-resolution impedance manometry (HRIM), and esophageal pH testing. Postoperative persistent dysphagia was defined as a postoperative score of > 3 for the dysphagia-specific item within the GERD-HRQL at a minimum of 3 months following MSA. A timeline of dysphagia and dilation rates was constructed and correlated with the evolution of our patient management practices and modifications in surgical technique. Results A total of 380 patients underwent MSA, at a mean (SD) follow up of 11.5 (8.7) months, 59 (15.5%) patients were experiencing persistent dysphagia. Thirty-one percent of patients required at least one dilation for dysphagia or chest pain and the overall response rate to this procedure was 67%, 7 (1.8%) patients required device removal specifically for dysphagia. Independent predictors of persistent dysphagia based on logistic regression model included (1) absence of a large hernia (OR 2.86 (95% CI 1.08-7.57, p = 0.035)); (2) the presence of preoperative dysphagia (OR 2.19 (95% CI 1.05-4.58, p = 0.037)); and (3) having less than 80% peristaltic contractions on HRIM (OR 2.50 (95% CI 1.09-5.73, p = 0.031)). Graded cutoffs of distal contractile integral (DCI), mean wave amplitude, DeMeester score, sex, and body mass index were evaluated within the model and did not predict postoperative dysphagia. Frequent eating after surgery, avoidance of early dilation, and increase in the size of the LINX device selected decreased the need for dilation. Conclusion In a large cohort of patients who underwent MSA, we report 15.5% rate of persistent postoperative dysphagia. The overall response rate to dilation therapy is 67%, and the efficacy of dilation with each subsequent procedure reduces. Patients with normal hiatal anatomy, significant preoperative dysphagia, and less than 80% peristaltic contractions of the smooth muscle portion of the esophagus should be counseled that they have an increased risk for persistent postoperative dysphagia.

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Dysbiosis and oxidative stress in the gut have contributed to the progression of intestinal inflammatory bowel disease (IBD). The current study has reported that enteric bacteria mediate redox homeostasis through the regulation of reactive oxygen species (ROS) production. Resveratrol, one of the most abundant polyphenols, with poor oral bioavailability, is considered as a scavenger of ROS and other free radicals. Recent studies have shown that resveratrol effectively enhances the growth of Lactococcus lactis and inhibits the growth of Enterococcus faecalis. (1) In terms of the two-way relationship between gut microbiota and resveratrol, resveratrol modulates gut microbiota; (2) in terms of resveratrol biotransformation by gut microbiota, we speculate that gut microbiota could be a target of resveratrol to maintain gut homeostasis. Here, we reviewed the current researches about the cellular signaling pathways in intestinal epithelial cells triggered by gut microbiota in response to oxidative stress. These results suggest that the modulation of the gut microbiota through resveratrol supplementation appears as a promising potential approach for the therapy of inflammatory bowel disease.

Administration of probiotics before or after standard triple therapy may improve H. pylori eradication rates.

The fact that oxymatrine can reduce the serum levels of TNF-alpha, IL-6, and the expression of NF-kappaB and ICAM-1 in colonic mucosa in DSS-induced colitis of rats indicates that oxymatrine may ameliorate the colonic inflammation and thus alleviate diarrhea and bloody stool.

AIMTo explore the mechanism by which microRNA-155 (miR-155) regulates the pathogenesis of experimental colitis.METHODSA luciferase assay was performed to confirm the binding of miR-155 to the SHIP-1 3’-UTR. MiR-155 mimics, negative controls and SHIP-1 expression/knockdown vectors were established and then utilized in gain- and loss-of-function studies performed in raw264.7 cells and primary bone marrow-derived macrophages (BMDMs). Thereafter, dextran sulfate sodium (DSS)-induced colitis mouse model with or without antagomiR-155 treatment was established, and the levels of miR-155 and SHIP-1, as well as the pro-inflammatory capabilities, were measured by western blot, quantitative polymerase chain reaction, and immunohistochemistry.RESULTSMiR-155 directly bound to the 3’-UTR of SHIP-1 mRNA and induced a significant decrease in SHIP-1 expression in both raw264.7 cells and primary BMDMs. MiR-155 markedly promoted cell proliferation and pro-inflammatory secretions including IL-6, TNF-α, IL-1β, and IFN-γ, whereas these effects could be reversed by the restoration of SHIP-1 expression. In vivo studies showed that antagomiR-155 administration could alleviate DSS-induced intestinal inflammation in Balb/c mice. Moreover, significantly increased SHIP-1 expression, as well as decreased Akt activation and inflammatory response, were observed in the antagomiR-155-treated mice.CONCLUSIONMiR-155 promotes experimental colitis by repressing SHIP-1 expression. Thus, the inhibition of miR-155 might be a promising strategy for therapy.