ArticleThe Journal of pathology2015
CXCR2 inhibition suppresses acute and chronic pancreatic inflammation.
Article in The Journal of pathology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
39 citing papers in PubMed, 71 citations in OpenAlex.
- Evasins: Biology and Therapeutic Potential of Broad-Spectrum Chemokine Inhibitors.Basic & clinical pharmacology & toxicology · 2026Review
- Screening of Biomarkers Related to Mitophagy in Severe Pancreatitis Based on Bioinformatics Methods.Iranian journal of biotechnology · 2026Article
- CXCL8 greatly enhances neutrophil extracellular traps formation induced by calcium crystalsFrontiers in pharmacology · 2026Article
- Astragalin attenuates caerulein-induced acute pancreatitis by targeting the NLRP3 signaling pathway and gut microbiota.Bioresources and bioprocessing · 2025Article
- Potential causal association between gut microbiota, inflammatory cytokines, and acute pancreatitis: A Mendelian randomization study.Journal of intensive medicine · 2025Article
- Shear-Stress Initiates Signal Two of NLRP3 Inflammasome Activation in LPS-Primed Macrophages through Piezo1.ACS applied materials & interfaces · 2025Article
- Article
- Inhibition of ADAM17 attenuates high glucose-induced angiogenesis and inflammation in endothelial cells partly through down-regulation of GRO-α/CXCR2 expression: implications in peritoneal dialysis.Clinical and experimental nephrology · 2024Article
- Characterizing Neutrophil Subtypes in Cancer Using scRNA Sequencing Demonstrates the Importance of IL1β/CXCR2 Axis in Generation of Metastasis-specific Neutrophils.Cancer research communications · 2024Article
- Non-coding RNAs and Exosomal Non-coding RNAs in Traumatic Brain Injury: the Small Player with Big Actions.Molecular neurobiology · 2023Review
- Immune cells and immune cell-targeted therapy in chronic pancreatitis.Frontiers in oncology · 2023Review
- Article
- Improvement in insulin sensitivity and prevention of high fat diet-induced liver pathology using a CXCR2 antagonist.Cardiovascular diabetology · 2022Article
- Neutrophils as potential therapeutic targets in hepatocellular carcinoma.Nature reviews. Gastroenterology & hepatology · 2022Review
- Loss ofBladder cancer (Amsterdam, Netherlands) · 2022Article
- Lipopeptide Pepducins as Therapeutic Agents.Methods in molecular biology (Clifton, N.J.) · 2022Article
- CXCR2 Is Essential for Radiation-Induced Intestinal Injury by Initiating Neutrophil Infiltration.Journal of immunology research · 2022Article
- Neutrophils in pancreatic cancer: Potential therapeutic targets.Frontiers in oncology · 2022Review
- Article
- Gain-of-function p53Cell reports · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
Abstract
Pancreatitis is a significant clinical problem and the lack of effective therapeutic options means that treatment is often palliative rather than curative. A deeper understanding of the pathogenesis of both acute and chronic pancreatitis is necessary to develop new therapies. Pathological changes in pancreatitis are dependent on innate immune cell recruitment to the site of initial tissue damage, and on the coordination of downstream inflammatory pathways. The chemokine receptor CXCR2 drives neutrophil recruitment during inflammation, and to investigate its role in pancreatic inflammation, we induced acute and chronic pancreatitis in wild-type and Cxcr2(-/-) mice. Strikingly, Cxcr2(-/-) mice were strongly protected from tissue damage in models of acute pancreatitis, and this could be recapitulated by neutrophil depletion or by the specific deletion of Cxcr2 from myeloid cells. The pancreata of Cxcr2(-/-) mice were also substantially protected from damage during chronic pancreatitis. Neutrophil depletion was less effective in this model, suggesting that CXCR2 on non-neutrophils contributes to the development of chronic pancreatitis. Importantly, pharmacological inhibition of CXCR2 in wild-type mice replicated the protection seen in Cxcr2(-/-) mice in acute and chronic models of pancreatitis. Moreover, acute pancreatic inflammation was reversible by inhibition of CXCR2. Thus, CXCR2 is critically involved in the development of acute and chronic pancreatitis in mice, and its inhibition or loss protects against pancreatic damage. CXCR2 may therefore be a viable therapeutic target in the treatment of 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.