Agent In Pancreatitis Research Articles

Detection and Typing of a Fowl Adenovirus Type 1 Agent of Pancreatitis in Guinea Fowl.

Adenoviral pancreatitis has been amply described for decades in guinea fowl. Although its pathologic picture has been characterized fairly well, its etiology still remains only partially clarified. Based on several outbreaks diagnosed on commercial guinea flocks raised in France since 2017, we performed direct whole-genome sequencing from pancreatic lesional tissue by using the Oxford Nanopore Technologies (ONT) sequencing method. We generated 4781 viral reads and assembled a whole genome of 43,509 bp, clustering within fowl adenovirus type 1 (FAdV-1). A phylogenetic analysis based on a partial sequence of the hexon and short fiber genes on viruses collected in France showed 98.7% and 99.8% nucleotide identity, respectively. Altogether, these results confirm that an FAdV-1 closely related to chicken and other avian strains is the agent of pancreatitis in guinea fowl. This study illustrates the potential of ONT sequencing method to achieve rapid whole-genome sequencing directly from pathologic material.

Gallstone and alcoholic pancreatitis? Evaluation of Atlanta and determinant based classification scores

We have previously demonstrated that pterostilbene, a compound in blueberries, exerts antiproliferative effects against pancreatic adenocarcinoma. However, little is known about the anti-inflammatory effects of pterostilbene in pancreatitis. Therefore, the aim of this study was to evaluate the effect of pterostilbene on inflammatory markers in an in vitro pancreatitis model. We hypothesized that pterostilbene would ameliorate the immediate inflammatory response in tumor necrosis factor alpha (TNF-α)–induced pancreatitis through downregulation of signal transducer and activator of transcription 3 (STAT3) and inhibition of TNF-α–induced secretion of lipase and proinflammatory cytokines interleukins (ILs) 1β and 6.AR42J acinar cells were pretreated with TNF-α to induce pancreatitis followed by 25 and 50 μM pterostilbene for 15 and 30 min. Secretion of lipase was quantified using a lipase assay and used as a marker of TNF-α–induced pancreatitis. Detection of STAT3, IL-1β, and IL-6 was performed using enzyme-linked immunosorbent assay. Analysis of variance and Tukey post hoc analysis were used for statistical analysis.TNF-α increased the secretion of lipase, IL-1β, and IL-6. Pterostilbene treatment inhibited TNF-α–induced secretion of lipase (P < 0.01 and P < 0.001), IL-1β (P < 0.05), and IL-6 (P < 0.05 and P < 0.01). Inhibition of STAT3 by pterostilbene occurred with treatment doses of 25 and 50 μM (P < 0.001 and P < 0.01).The dietary compound pterostilbene exerts an anti-inflammatory effect in pancreatitis through downregulation of STAT3 and decreased the secretion of lipase, IL-1β, and IL-6. Pterostilbene's amelioration of pancreatitis in vitro makes it an advantageous anti-inflammatory agent. Further studies are necessary to determine pterostilbene's role as a protective or therapeutic agent in pancreatitis.

Pterostilbene ameliorates tumor necrosis factor alpha–induced pancreatitis in vitro

BackgroundWe have previously demonstrated that pterostilbene, a compound in blueberries, exerts antiproliferative effects against pancreatic adenocarcinoma. However, little is known about the anti-inflammatory effects of pterostilbene in pancreatitis. Therefore, the aim of this study was to evaluate the effect of pterostilbene on inflammatory markers in an in vitro pancreatitis model. We hypothesized that pterostilbene would ameliorate the immediate inflammatory response in tumor necrosis factor alpha (TNF-α)–induced pancreatitis through downregulation of signal transducer and activator of transcription 3 (STAT3) and inhibition of TNF-α–induced secretion of lipase and proinflammatory cytokines interleukins (ILs) 1β and 6. MethodsAR42J acinar cells were pretreated with TNF-α to induce pancreatitis followed by 25 and 50μM pterostilbene for 15 and 30min. Secretion of lipase was quantified using a lipase assay and used as a marker of TNF-α–induced pancreatitis. Detection of STAT3, IL-1β, and IL-6 was performed using enzyme-linked immunosorbent assay. Analysis of variance and Tukey post hoc analysis were used for statistical analysis. ResultsTNF-α increased the secretion of lipase, IL-1β, and IL-6. Pterostilbene treatment inhibited TNF-α–induced secretion of lipase (P<0.01 and P<0.001), IL-1β (P<0.05), and IL-6 (P<0.05 and P<0.01). Inhibition of STAT3 by pterostilbene occurred with treatment doses of 25 and 50μM (P<0.001 and P<0.01). ConclusionsThe dietary compound pterostilbene exerts an anti-inflammatory effect in pancreatitis through downregulation of STAT3 and decreased the secretion of lipase, IL-1β, and IL-6. Pterostilbene's amelioration of pancreatitis in vitro makes it an advantageous anti-inflammatory agent. Further studies are necessary to determine pterostilbene's role as a protective or therapeutic agent in pancreatitis.

Gene therapy for pancreatitis pain

Pancreatic cancer and chronic pancreatitis are clinical syndromes associated with severe pain that is difficult to manage. Thus, seeking additional pain reduction therapies is warranted. Excessive alcohol consumption over an extended period of time is the primary causal agent in pancreatitis. The efficacy of a replication defective Herpes (HSV-1, DPE) viral vector construct encoding the human preproenkephalin gene (HSV-Enk), used as a molecular therapy for alleviation of pancreatitis pain, is reviewed here. The characteristics of the gene therapy treatment for inflammation and pain-related behavior in two alcoholic pancreatitis animal models is described. Significant analgesia and protection of pancreatic tissue was provided for the duration of the transgene expression (approximately 4-6 weeks). These studies establish a basis for use of HSV-based gene therapy for chronic visceral pain. Targeted enkephalin gene therapy approaches are providing clear promise for pain control. As innovative means of significantly reducing pancreatic inflammation and preserving tissue architecture, they may extend their clinical usefulness for pancreatitis and pancreatic cancer pain patients.

Different Inhibitory Effects of the Newly Developed CCK Receptor Antagonists FK480 and KSG-504 on Pancreatic Exocrine and Endocrine Secretion in the Isolated Perfused Rat Pancreas

Cholecystokinin (CCK) receptor antagonists are shown to have therapeutic as well as preventive effects in some types of acute pancreatitis. However, there is a possibility that administration of CCK receptor antagonists with a high inhibitory potency on the endocrine pancreas to patients with acute pancreatitis exacerbates the associated glucose intolerance. In the present study we simultaneously examined the effects of the newly developed benzodiazepine derivative FK480 and proglumide-related antagonist KSG-504 on CCK octapeptide (CCK-8)-stimulated exocrine and endocrine function in the isolated perfused rat pancreas. FK480 and KSG-504 inhibited CCK-8-stimulated pancreatic juice flow, protein output, and insulin release in a dose-dependent manner. FK480 was approximately 10 times more potent than KSG-504 in inhibiting exocrine and endocrine secretion. Both antagonists inhibited CCK-8-stimulated insulin release more potently than exocrine secretion. FK480 caused a dose-dependent residual inhibition of exocrine secretion after its removal from the perfusate, whereas insulin release was only slightly impaired even at the highest dose. In contrast, termination of KSG-504 infusion resulted in an immediate increase in both exocrine and insulin responses without causing any residual inhibition. With regard to the residual inhibition, therefore, KSG-504 had no significant influences on exocrine and insulin release, whereas FK480 inhibited exocrine secretion more potently than insulin response. These results suggest that FK480 might become a useful therapeutic agent for pancreatitis with respect to its long-duration inhibitory effect on exocrine secretion and short-duration inhibitory effect on insulin release.

Transitory elevation of serum amylase levels after restorative proctocolectomy.

The incidence of postoperative hyperamylasaemia was evaluated in 70 patients who underwent staged restorative proctocolectomy. On the 14th postoperative day, 27 of 70 patients after total colectomy showed hyperamylasaemia, and the serum amylase returned to normal on the 30th postoperative day. Three out of 37 after ileoanal anastomosis and 8 out of 70 after stoma closure showed elevation of serum amylase postoperatively. Total colectomy might have a possible role in the postoperative increase of serum amylase. None of these patients had any obvious clinical evidence of postoperative pancreatitis. In 7 patients showing significant elevation of serum amylase levels (over 1000 IU), this was due predominantly to the pancreatic isoenzyme. This transitory elevation of serum amylase did not seem to be altered by the administration of therapeutic agents for pancreatitis. These observations suggest that postoperative hyperamylasaemia without clinical evidence of pancreatitis is very common after total colectomy, and that postoperative hyperamylasaemia itself does not necessarily require treatment.