ArticleGastroenterology2016
Aryl Hydrocarbon Receptor Ligands in Cigarette Smoke Induce Production of Interleukin-22 to Promote Pancreatic Fibrosis in Models of Chronic Pancreatitis.
Article in Gastroenterology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.
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Who cites it
70 citing papers in PubMed, 150 citations in OpenAlex.
- Reduction of inflammation in chronic pancreatitis using a soy bread intervention: A feasibility study.Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.] · 2020Trial
- Collaborative functionality between three types of inflammation in idiopathic pulmonary fibrosis.Nature immunology · 2026Review
- Gut microbiota-derived metabolites as immune modulators in aging and age-related chronic inflammatory diseases.Ageing research reviews · 2026Review
- Aryl Hydrocarbon Receptor Ligands Drive Pancreatic Cancer Initiation and Progression through Protumorigenic T-cell Polarization.Cancer discovery · 2026Article
- Craniofacial and dental toxicity of dioxins: developmental phenotypes and mechanistic insights.Frontiers in cell and developmental biology · 2026Review
- Transcriptional Activity of Genes Related to the Biotransformation Process in the Development of Colorectal Cancer.International journal of molecular sciences · 2025Article
- Activation of the aryl hydrocarbon receptor relieves acute pancreatitis via the RBX1/HSF1 pathway.Journal of inflammation (London, England) · 2025Article
- Impact of E-Cigarette Vapor and Cigarette Smoke on Brain Expression of ABCB1 and ABCG2 Efflux Transporters.Neurochemical research · 2025Article
- Risk factors for visceral artery pseudoaneurysm in chronic pancreatitis: A retrospective analysis.Turkish journal of surgery · 2025Article
- Pancreatic atrophy after gastric cancer surgery: influencing factors and effects on BMI and quality of life.World journal of surgical oncology · 2025Article
- PdgfrαGenes & diseases · 2025Review
- Risk factors for calcification in chronic pancreatitis: a systematic review and meta-analysis.Frontiers in medicine · 2025Article
- Impact of Elevated Serum Triglycerides on Children with Acute Recurrent or Chronic Pancreatitis from INSPPIRE-2.The Journal of pediatrics · 2025Article
- Pancreatic stellate cells and the interleukin family: Linking fibrosis and immunity to pancreatic ductal adenocarcinoma (Review).Molecular medicine reports · 2024Review
- Tumour-associated myeloid cells expressing IL-10R2/IL-22R1 as a potential biomarker for diagnosis and recurrence of pancreatic ductal adenocarcinoma.British journal of cancer · 2024Article
- The Role of Endocrine Disruption Chemical-Regulated Aryl Hydrocarbon Receptor Activity in the Pathogenesis of Pancreatic Diseases and Cancer.International journal of molecular sciences · 2024Review
- Activation and Regulation of Pancreatic Stellate Cells in Chronic Pancreatic Fibrosis: A Potential Therapeutic Approach for Chronic Pancreatitis.Biomedicines · 2024Review
- Single-Cell Sequencing Data Analysis Unveiled HDAC1 as the Therapeutic Target for Chronic Pancreatitis.Molecular biotechnology · 2024Article
- Distinct fibroblast functions associated with fibrotic and immune-mediated inflammatory diseases and their implications for therapeutic development.F1000Research · 2024Review
- Article
10 more citing papers are in PubMed but not listed here.
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
Abstract
BACKGROUND &
aimsCigarette smoke has been identified as an independent risk factor for chronic pancreatitis (CP). Little is known about the mechanisms by which smoking promotes development of CP. We assessed the effects of aryl hydrocarbon receptor (AhR) ligands found in cigarette smoke on immune cell activation in humans and pancreatic fibrosis in animal models of CP.
methodsWe obtained serum samples from patients with CP treated at Stanford University hospital and healthy individuals (controls) and isolated CD4
resultsMice given AhR agonists developed more severe pancreatic fibrosis (based on decreased pancreas size, histology, and increased expression of fibrosis-associated genes) than mice not given agonists after caerulein injection. In mice given saline instead of caerulein, AhR ligands did not induce fibrosis. Pancreatic T cells from mice given AhR agonists and caerulein were activated and expressed IL22, but not IL17 or interferon gamma. Human T cells exposed to AhR agonists up-regulated expression of IL22. In mice given anti-IL22, pancreatic fibrosis did not progress, whereas mice given recombinant IL22 had a smaller pancreas and increased fibrosis. Pancreatic stellate cells isolated from mouse and human pancreata expressed the IL22 receptor IL22RA1. Incubation of the pancreatic stellate cells with IL22 induced their expression of the extracellular matrix genes fibronectin 1 and collagen type I α1 chain, but not α2 smooth muscle actin or transforming growth factor-β. Serum samples from smokers had significantly higher levels of IL22 than those from nonsmokers.
conclusionsAhR ligands found in cigarette smoke increase the severity of pancreatic fibrosis in mouse models of pancreatitis via up-regulation of IL22. This pathway might be targeted for treatment of CP and serve as a biomarker of disease.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.