Abstract
Pancreatitis, a debilitating inflammatory disorder, results from pancreatic injury. Alcohol abuse is the foremost cause, although cigarette smoking has recently surfaced as a distinct risk factor. The mechanisms by which cigarette smoke and its toxins initiate pathological cellular events leading to pancreatitis, have not been clearly defined. Although cigarette smoke is composed of more than 4000 compounds, it is mainly nicotine and the tobacco-specific nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), which have been extensively studied with respect to pancreatic diseases. This review summarizes these research findings and highlights cellular pathways which may be of relevance in initiation and progression of smoking-related pancreatitis.
Highlights
Pancreatitis is an inflammatory condition which arises following injury to the pancreas
The amount of knowledge regarding the pathogenesis of smoking-induced pancreatitis is scarce compared with what is known about other etiologies of the disease, such as alcohol abuse and gallstones
Some models described in this review, which focus on specific cigarette toxins, such as nicotine and it’s more potent derivative NNK, have yielded encouraging findings
Summary
Pancreatitis is an inflammatory condition which arises following injury to the pancreas. An early pivotal event in initiation of acute pancreatitis (AP) is premature activation and retention of digestive pro-enzymes (zymogens) in pancreatic acinar cells, leading to autodigestion of the pancreas [1]. Recurrent bouts of AP can set in motion inflammatory events that in turn lead to stellate cell activation and increased fibrosis, resulting in chronic pancreatitis (CP) [3]. Some scientific studies have investigated effects of cigarette smoke inhalation in rats; animals developed pancreatic injury and elevated levels of pancreatic zymogens, the cellular damage was less than that observed in human CP [18,19]. We will further explore recent research looking at effects and mechanisms mediated by nicotine and the tobacco-specific nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), and their potential role in development of pancreatitis
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