Intestinal inflammation is associated with various pathological diseases, such as gastritis from Helicobacter pylori infection, Crohn's and colitis in inflammatory bowel disease, and colorectal cancer. Thus, treatment with anti-inflammatory substances in these inflammation-associated diseases is critical. Increasingly compelling evidence indicates that glutamine is an anti-inflammatory compound candidate because it can influence the long-term outcome of the inflammatory diseases with in a low-risk way. However, before recommending its use in clinical practice, it is important to elucidate the molecular mechanism by which glutamine exerts its roles in modulating intestinal inflammation. In this study, we review the current knowledge on the detailed regulation pathway used by glutamine in its proinflammatory regulation, with a special emphasis on intestinal inflammation. These regulation pathways include nuclear factor kappa B (NF-κB), signal transducer and activator of transcription (STAT), mitogen-activated protein kinases (MAPK), phosphoinositide-3-kinases (PI3K)/PI3K-protein kinase B (Akt), activating protein-1 (AP-1), nitric oxide synthases (NOS)-nitric oxide (NO), peroxisome proliferator-activated receptor-Γ (PPARγ), heat shock factor-1 (HSF-1)- heat shock proteins (HSP) and glutathione (GSH) - reactive oxygen species (ROS). Although some regulatory pathways, such as PI3K/PI3K-Akt, GSH-ROS and AP-1, need to be further investigated, this review provides useful information to utilize glutamine as an immunonutritional or pharmaconutritional drug, not only for inflammation-associated diseases in the intestine, but also possibly for other inflammatory-associated diseases, i.e. arthritis, asthma, type 2 diabetes, etc.

Background: To explore significance of CA19-9, D-dimer with TNFAIP3 (A20) protein and evaluate its prognostic significance in patients suffering from pancreatic ductal adenocarcinoma (PDAC). Methods: 148 patients suffering from pancreatic ductal adenocarcinoma in Northern Jiangsu People’s Hospital affiliated to Yangzhou University between January 2012 to December 2016 were studied. Cutoff values of prognostic factors were predicted by Receiver operating characteristic curve (ROC curve). Kaplan-Meier method was used to describe survival curve of patients. Univariate and multivariate regression analyses were used to analyze prognostic factors of patients. Results: The recommended cutoff values of the neutrophil-lymphocyte rate (NLR), platelet-lymphocyte rate (PLR), CA19-9 and D-dimer were 2.04 (sensitivity, 0.59; specificity, 0.9; area under the ROC curve (AUC), 0.749; P<0.001), 52.94 (sensitivity, 0.73; specificity, 0.95; AUC, 0.829; P<0.001), 176.66U/ml (sensitivity, 0.7; specificity, 0.9; AUC, 0.794; P<0.001) and 1.18mg/L (sensitivity, 0.82; specificity, 0.9; AUC, 0.845; P<0.001) respectively. The expression of CA19-9 in serum was related with lymph node metastasis (P = 0.010), tumor lymph node metastasis (TNM) stage (P <0.001) and survival ratio (P <0.001). The D-dimer was positively related with differentiation grade (P=0.014), tumor size (P=0.045), TNM stage (P=0.006) and survival ratio (P<0.001). A20 was positively related with differentiation grade (P<0.001), BMI (P<0.001), TNM stage (P=0.024) and survival ratio (P<0.001). The Kaplan-Meier curves showed that the patients with pancreatic ductal adenocarcinoma had a significant difference in the expression of CA19-9 group, expression of D-dimer group and expression of A20 (P<0.05). CA19-9, D-dimer, TNM stage, differentiation grade and A20 were independent prognostic markers for patients sufferingfrom pancreatic ductal adenocarcinoma by univariate and COX multivariate analyses. Conclusions: CA19-9, D-dimer and A20 were independent prognostic markers for pancreatic ductal adenocarcinoma patients.