Sterile Inflammatory Response in Acute Pancreatitis

Effect of Ageing on Systemic Inflammatory Response in Acute Pancreatitis

Elderly patients show increased incidence of multiple organ dysfunction in acute pancreatitis possibly due to bacterial translocation. This is associated with increased susceptibility to infections in older people. Several reports have related this increased susceptibility to a proinflammatory status called inflammaging, which decreases the capacity of the immunological system to respond to ant...

Action of antiproteases on the inflammatory response in acute pancreatitis.

The spectrum of acute pancreatitis ranges from mild edematous disease to a severe necrotizing process which is usually accompanied by local or systemic complications and even mortality. Early deaths (within the first week) due to severe acute pancreatitis are generally caused by massive inflammatory responses which result in multiple organ failure. Although the exact mechanisms which trigger th...

Initiation of Experimental Acute Pancreatitis and Modulation of Inflammatory Response

flow cytometric analysis of inflammatory cells in experimental acute pancreatitis

background: accumulating evidence indicates that inflammatory cells migrate into the pancreas tissue and play an important role in the pathogenesis of acute pancreatitis (ap). the aim of this study was to establish a flow cytometric method to enumerate these infiltrating cells in the pancreas of an experimental ap. materials and methods: twelve hours after inducing of ap, mice pancreatic tissue...

Uric acid promotes an acute inflammatory response to sterile cell death in mice.

Necrosis stimulates inflammation, and this response is medically relevant because it contributes to the pathogenesis of a number of diseases. It is thought that necrosis stimulates inflammation because dying cells release proinflammatory molecules that are recognized by the immune system. However, relatively little is known about the molecular identity of these molecules and their contribution ...