ArticleJournal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract
Specific pancreatic enzymes activate macrophages to produce tumor necrosis factor-alpha: role of nuclear factor kappa B and inhibitory kappa B proteins.
Article in Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 49 citations in OpenAlex.
- Acute pancreatitis: mechanisms and therapeutic approaches.Signal transduction and targeted therapy · 2026Review
- The Role of Pancreatic Infiltrating Innate Immune Cells in Acute Pancreatitis.International journal of medical sciences · 2021Review
- Two to Tango: Dialogue between Adaptive and Innate Immunity in Type 1 Diabetes.Journal of diabetes research · 2020Review
- Bidirectional Relationship Between Reduced Blood pH and Acute Pancreatitis: A Translational Study of Their Noxious Combination.Frontiers in physiology · 2018Article
- Targeting MicroRNA Function in Acute Pancreatitis.Frontiers in physiology · 2017Review
- Pancreatic Acinar Cells Employ miRNAs as Mediators of Intercellular Communication to Participate in the Regulation of Pancreatitis-Associated Macrophage Activation.Mediators of inflammation · 2016Article
- Controversial role of toll-like receptors in acute pancreatitis.World journal of gastroenterology · 2013Review
- TNF-alpha-dependent regulation of acute pancreatitis severity by Ly-6C(hi) monocytes in mice.The Journal of biological chemistry · 2011Article
- Role of macrophages in the progression of acute pancreatitis.World journal of gastrointestinal pharmacology and therapeutics · 2010Article
- Use of gene expression profiles in cells of peripheral blood to identify new molecular markers of acute pancreatitis.Archives of surgery (Chicago, Ill. : 1960) · 2008Article
- Protein kinase C-zeta is critical in pancreatitis-induced apoptosis of Kupffer cells.Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract · 2007Article
- A nuclear import inhibitory peptide ameliorates the severity of cholecystokinin-induced acute pancreatitis.World journal of gastroenterology · 2005Article
- Pancreatic elastase induces liver injury by activating cytokine production within Kupffer cells via nuclear factor-Kappa B.Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary TractArticle
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The triggering events by which mononuclear cells throughout the body are induced to produce large amounts of cytokines during acute pancreatitis are unclear. However, recent work in our laboratory demonstrated that three specific pancreatic enzymes (elastase, carboxypeptidase A, and lipase) induced dramatic tumor necrosis factor-alpha (TNF-alpha) protein production from macrophages, whereas all others could not. This series of experiments was designed to examine the second messenger system by which this occurs. The rat macrophage cell line NR8383 was incubated for 3 hours with elastase, carboxypeptidase A, lipase, trypsin, or lipopolysaccharide (positive control). Activation of nuclear factor kappa B (NF-kappa B) was demonstrated by electrophoretic mobility shift assay, presence of inhibitory kappa B alpha and beta (I kappa B-alpha and I kappa B-beta) by Western blot analysis, and TNF-alpha protein production by enzyme-linked immunosorbent assay. Elastase, carboxypeptidase A, and lipase induced degradation of I kappa B-beta (but not I kappa B-alpha), activation of NF-kappa B, and production of TNF-alpha protein, whereas inhibition of I kappa B with pyrrolidine dithiocarbamate attenuated this response. Trypsin was unable to elicit any of these responses. Macrophages can be induced by specific activated pancreatic enzymes-elastase, carboxypeptidase A, and lipase-to produce TNF-alpha. This process is dependent on I kappa B-beta degradation and NF- kappa B activation, suggesting that these enzymes trigger this second messenger system through specific membrane-bound receptors.
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