ReviewJournal of inflammation (London, England)2022
The immunological function of CXCR2 in the liver during sepsis.
Review in Journal of inflammation (London, England), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
11 citing papers in PubMed, 13 citations in OpenAlex.
- Inhibiting CXCR2 Remodels the Tumor Microenvironment and Blunts Tumor Progression and Dissemination of High-Grade Serous Carcinoma.Cancer research communications · 2026Article
- Polymicrobial Sepsis-Induced Changes in Hepatic Stellate Cell Communication in Male C57BL/6J Mice.Cells · 2026Article
- Interleukin-39 aggravates sepsis by inducing self-sustaining neutrophil activation in the lungs via the CXCL1-CXCR2 pathway.International journal of biological sciences · 2026Article
- BDKRB1 activation induces CXCR2 desensitization in neutrophils during severe sepsis and exacerbates disease severity.JCI insight · 2025Article
- The peptide genomic therapy increases antibacterial immunity and survival in sepsis by reprograming the gene orthologs of human immunodeficiencies in the spleen and lungs.Frontiers in immunology · 2025Article
- The dual role of neutrophils in sepsis-associated liver injury.Frontiers in immunology · 2025Review
- CXCR4 antagonism corrects neutrophil abnormalities and reduces pneumonia severity in a pharmacological mouse model of CXCR2 loss-of-function-mediated neutropenia.Frontiers in immunology · 2025Article
- Inhibition of IL-27 signaling regulates chemokine levels and sustains CXCR2 receptor expression on mononuclear cells to improve disease outcomes during gram-negative neonatal sepsis.Frontiers in immunology · 2025Article
- Identification of Co-Diagnostic Genes and Potential Therapeutic Targets for Asthma and Sepsis Through Mendelian Randomization and Immune Infiltration Analysis.Journal of asthma and allergy · 2025Article
- Transcriptional pathways of terminal differentiation in high- and low-density blood granulocytes in sepsis.Journal of inflammation (London, England) · 2024Article
- Novel Anti-Enterovirus A71 Compounds Discovered by Repositioning Antivirals from the Open-Source MMV Pandemic Response Box.Pharmaceuticals (Basel, Switzerland) · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
backgroundThe chemokine receptor CXCR2 and its ligands, especially CXCL8, are crucial mediators for the progression of liver inflammation and liver failure in sepsis. Neutrophils have the highest CXCR2 expression in mice and humans, and their activation via CXCL8 facilitates their migration to the inflamed liver for the clearance of the pathogens and, in turn, the inflammation. MAIN BODY: In sepsis, the inflammatory insult causes extensive neutrophil migration to the liver that overwhelms the immune response. To compensate for the strong receptor activation, CXCR2 desensitizes, incapacitating the immune cells to efficiently clear pathogens, causing further life-threatening liver damage and uncontrolled pathogen spread.
conclusionCXCR2 function during infection strongly depends on the expressing cell type. It signals pro- and anti-inflammatory effects that may prompt novel cell-type-specific CXCR2-directed therapeutics.
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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.