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The premature intracellular activation of digestive proteases can result in autodigestion of the pancreas and has long been regarded as the initial and a rate-limiting step in the development of acute pancreatitis.1 Recent evidence suggests, however, that inflammatory cells infiltrating the pancreas—rather than the extent of initial protease activation—determines the ultimate severity of acute pancreatitis.2 3 All attempts to target the inflammatory response of acute pancreatitis therapeutically have unfortunately been unsuccessful. One reason for this failure may lie in the type of inflammatory cells that were targeted.4
Macrophages orchestrate both the initiation and the resolution of inflammation and would therefore be an interesting therapeutic target for modulating the inflammatory response in acute pancreatitis. Selective depletion of the proinflammatory M1 macrophages has been found to reduce the severity in acute pancreatitis.5
Nature has provided a potent protective strategy to counter an overwhelming inflammatory response. Haemoxygenase-1 (HO-1) is an inducible isoform of the initial and rate-controlling enzyme used in the degradation of haem into iron, carbon monoxide and biliverdin. The latter is subsequently converted to bilirubin.6 HO-1 is expressed in various inflammatory cells including macrophages and has recently gained considerable attention for exerting …
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