ArticleThe Journal of biological chemistry2011
TNF-alpha-dependent regulation of acute pancreatitis severity by Ly-6C(hi) monocytes in mice.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 56 citations in OpenAlex.
- Disrupted endocannabinoid signaling contributes to systemic inflammation in acute pancreatitis.The Journal of pathology · 2026Article
- IL-4/STAT6-signaling Influences Local Inflammation and Regeneration Processes During Acute Pancreatitis and Promotes Fibrosis by a Direct Activation of Pancreatic Fibroblasts During Chronic Pancreatitis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Role of Interleukin-6 Mediated T Cell Activation in Experimental Acute Pancreatitis.Inflammation · 2025Article
- Global insights and knowledge mapping of immunity and inflammation in acute pancreatitis: A bibliometric and visual analysis.Medicine · 2025Article
- Gene Regulation of Neutrophils Mediated Liver and Lung Injury through NETosis in Acute Pancreatitis.Inflammation · 2025Article
- Overview of the cellular and immune mechanisms involved in acute pancreatitis: In search of new prognosis biomarkers.Expert reviews in molecular medicine · 2025Review
- IRAK3-mediated suppression of pro-inflammatory MyD88/IRAK signaling affects disease severity in acute pancreatitis.Scientific reports · 2023Article
- Article
- JMJD3 Is Required for Acute Pancreatitis and Pancreatitis-Associated Lung Injury.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- Immune response mechanisms in acute and chronic pancreatitis: strategies for therapeutic intervention.Frontiers in immunology · 2023Review
- Pirfenidone increases IL-10 and improves acute pancreatitis in multiple clinically relevant murine models.JCI insight · 2022Article
- Roles, detection, and visualization of neutrophil extracellular traps in acute pancreatitis.Frontiers in immunology · 2022Review
- Circulating monocytes in acute pancreatitis.Frontiers in immunology · 2022Review
- Novel Circulating and Tissue Monocytes as Well as Macrophages in Pancreatitis and Recovery.Gastroenterology · 2021Article
- Betulinic Acid Ameliorates the Severity of Acute Pancreatitis via Inhibition of the NF-κB Signaling Pathway in Mice.International journal of molecular sciences · 2021Article
- Tumor-Associated Macrophages in Pancreatic Ductal Adenocarcinoma: Therapeutic Opportunities and Clinical Challenges.Cancers · 2021Review
- The Role of Pancreatic Infiltrating Innate Immune Cells in Acute Pancreatitis.International journal of medical sciences · 2021Review
- Modulation of macrophage polarity for treatment of acute pancreatitis: Are we there yet?EBioMedicine · 2020Article
- ANGPTL4 exacerbates pancreatitis by augmenting acinar cell injury through upregulation of C5a.EMBO molecular medicine · 2020Article
- Absence of the neutrophil serine protease cathepsin G decreases neutrophil granulocyte infiltration but does not change the severity of acute pancreatitis.Scientific reports · 2019Article
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
The roles of monocytes/macrophages and their mechanisms of action in the regulation of pancreatitis are poorly understood. To address these issues, we have employed genetically altered mouse strains that either express the human diphtheria toxin receptor (DTR) coupled to the CD11b promoter or have global deletion of TNF-α. Targeted, conditional depletion of monocytes/macrophages was achieved by administration of diphtheria toxin (DT) to CD11b-DTR mice. We show that in the absence of DT administration, pancreatitis is associated with an increase in pancreatic content of Ly-6C(hi) monocytes/macrophages but that this response is prevented by prior administration of DT to CD11b-DTR mice. DT administration also reduces pancreatic edema and acinar cell injury/necrosis in two dissimilar experimental models of acute pancreatitis (a secretagogue-induced model and a model elicited by retrograde pancreatic duct infusion of sodium taurocholate). In the secretagogue-elicited model, the DT-induced decrease in pancreatitis severity is reversed by adoptive transfer of purified Ly-6C(hi) monocytes harvested from non-DT-treated CD11b-DTR mice or by the transfer of purified Ly-6C(hi) monocytes harvested from TNF-α(+/+) donor mice, but it is not reversed by the transfer of Ly-6C(hi) monocytes harvested from TNF-α(-/-) donors. Our studies indicate that the Ly-6C(hi) monocyte subset regulates the severity of pancreatitis by promoting pancreatic edema and acinar cell injury/necrosis and that this phenomenon is dependent upon the expression of TNF-α by those cells. They suggest that therapies targeting Ly-6C(hi) monocytes and/or TNF-α expression by Ly-6C(hi) monocytes might prove beneficial in the prevention or treatment of acute pancreatitis.
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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.