TLR4 dependent heparan sulphate-induced pancreatic inflammatory response is IRF3-mediated.

Background: Degraded extracellular matrix can stimulate the innate immune system via the Toll-Like Receptor-4 (TLR4). In the pancreas, syndecan-anchored heparan sulphate (HS) on the ductal epithelium can be cleaved off its protein cores by the proteases (trypsin and elastase) and potentially activate TLR4 signalling.

Methods: To investigate this signalling event, a low sulphated HS (500 μg/ml) was infused into the biliary-pancreatic duct of C57BL/6J wild-type mice.

Proposed protective mechanism of the pancreas in the rat.

Background: Heparan sulphate is known to have various functions in the animal body, including surveillance of tissue integrity. Administered intraperitoneally, it induces a systemic inflammatory response syndrome and when given locally in the pancreas it initiates a protective inflammatory response. The aim of the present study was to investigate the underlying mechanisms behind cell recruitment following intra-ductal infusion of heparan sulphate.

Early nasogastric feeding in predicted severe acute pancreatitis: A clinical, randomized study.

Objective: To compare the efficacy and safety of early, nasogastric enteral nutrition (EN) with total parenteral nutrition (TPN) in patients with predicted severe acute pancreatitis (SAP).

Summary Background Data: In SAP, the magnitude of the inflammatory response as well as increased intestinal permeability correlates with outcome. Enteral feeding has been suggested superior to parenteral feeding due to a proposed beneficial effect on the gut barrier.