Cigarette Smoking Impairs Pancreatic Duct Cell Bicarbonate Secretion

Kadiyala, Vivek; Lee, Linda; Banks, Peter A.; Suleiman, Shadeah; Paulo, João A.; Wang, Wei; Rosenblum, Jessica; Sainani, Nisha I.; Mortelé, Koenraad J.; Conwell, Darwin L.

doi:10.6092/1590-8577/1195

Cited by 17 publications

(2 citation statements)

References 49 publications

(63 reference statements)

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“…Additionally, cigarette smoking initiates and/or propagates pro-inflammatory and pro-fibrotic pathways that contribute to reduced exocrine (and endocrine) function [ 50 ]. Furthermore, both alcohol consumption and smoking can impair CFTR function further contributing to the previously discussed ductal dysfunction [ 51 , 52 ].…”

Section: Pathophysiologymentioning

confidence: 99%

Alterations in exocrine pancreatic function after acute pancreatitis

Bejjani,

Ramsey,

Lee

et al. 2024

Pancreatology

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Section: Pathophysiologymentioning

confidence: 99%

Alterations in exocrine pancreatic function after acute pancreatitis

Bejjani,

Ramsey,

Lee

et al. 2024

Pancreatology

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“… 23 Studies on human subjects have shown that past and current smokers have decreased pancreatic HCO 3 − secretion, suggesting a dysfunction of the ductal epithelial cells when compared to never smokers. 24 , 25 Therefore, the aim of this study was to understand the effects and mechanism of smoking, one of the most important risk factors for CP, on pancreatic ductal epithelial cells (PDECs).…”

Section: Introductionmentioning

confidence: 99%

Heavy metals in cigarette smoke strongly inhibit pancreatic ductal function and promote development of chronic pancreatitis

Pallagi,

Tóth,

Görög

et al. 2024

Clinical & Translational Med

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Background and aimsSmoking is recognised as an independent risk factor in the development of chronic pancreatitis (CP). Cystic fibrosis transmembrane conductance regulator (CFTR) function and ductal fluid and bicarbonate secretion are also known to be impaired in CP, so it is crucial to understand the relationships between smoking, pancreatic ductal function and the development of CP.MethodsWe measured sweat chloride (Cl–) concentrations in patients with and without CP, both smokers and non‐smokers, to assess CFTR activity. Serum heavy metal levels and tissue cadmium concentrations were determined by mass spectrometry in smoking and non‐smoking patients. Guinea pigs were exposed to cigarette smoke, and cigarette smoke extract (CSE) was prepared to characterise its effects on pancreatic HCO3– and fluid secretion and CFTR function. We administered cerulein to both the smoking and non‐smoking groups of mice to induce pancreatitis.ResultsSweat samples from smokers, both with and without CP, exhibited elevated Cl– concentrations compared to those from non‐smokers, indicating a decrease in CFTR activity due to smoking. Pancreatic tissues from smokers, regardless of CP status, displayed lower CFTR expression than those from non‐smokers. Serum levels of cadmium and mercury, as well as pancreatic tissue cadmium, were increased in smokers. Smoking, CSE, cadmium, mercury and nicotine all hindered fluid and HCO3– secretion and CFTR activity in pancreatic ductal cells. These effects were mediated by sustained increases in intracellular calcium ([Ca2+]i), depletion of intracellular ATP (ATPi) and mitochondrial membrane depolarisation.ConclusionSmoking impairs pancreatic ductal function and contributes to the development of CP. Heavy metals, notably cadmium, play a significant role in the harmful effects of smoking.Key points Smoking and cigarette smoke extract diminish pancreatic ductal fluid and HCO3– secretion as well as the expression and function of CFTR Cd and Hg concentrations are significantly higher in the serum samples of smokers Cd accumulates in the pancreatic tissue of smokers

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CFTR: A New Horizon in the Pathomechanism and Treatment of Pancreatitis

Hegyi

Wilschanski

Muallem

et al. 2016

Reviews of Physiology, Biochemistry and Pharmacology

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Cystic fibrosis transmembrane conductance regulator (CFTR) is an ion channel that conducts chloride and bicarbonate ions across epithelial cell membranes. Mutations in the CFTR gene diminish the ion channel function and lead to impaired epithelial fluid transport in multiple organs such as the lung and the pancreas resulting in cystic fibrosis. Heterozygous carriers of CFTR mutations do not develop cystic fibrosis but exhibit increased risk for pancreatitis and associated pancreatic damage characterized by elevated mucus levels, fibrosis and cyst formation. Importantly, recent studies demonstrated that pancreatitis causing insults, such as alcohol, smoking or bile acids strongly inhibit CFTR function. Furthermore, human studies showed reduced levels of CFTR expression and function in all forms of pancreatitis. These findings indicate that impairment of CFTR is critical in the development of pancreatitis; therefore, correcting CFTR function could be the first specific therapy in pancreatitis. In this review, we summarize recent advances in the field and discuss new possibilities for the treatment of pancreatitis.

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Cigarette Smoking Impairs Pancreatic Duct Cell Bicarbonate Secretion

Cited by 17 publications

References 49 publications

Alterations in exocrine pancreatic function after acute pancreatitis

Alterations in exocrine pancreatic function after acute pancreatitis

Heavy metals in cigarette smoke strongly inhibit pancreatic ductal function and promote development of chronic pancreatitis

CFTR: A New Horizon in the Pathomechanism and Treatment of Pancreatitis

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