ArticleeLife2022
A neutrophil-B-cell axis impacts tissue damage control in a mouse model of intraabdominal bacterial infection via Cxcr4.
Article in eLife, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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Who cites it
12 citing papers in PubMed, 16 citations in OpenAlex.
- A novel host-based strategy for detecting low-grade prosthetic joint infection using immune cell pattern in synovial fluid.Molecular medicine (Cambridge, Mass.) · 2026Article
- Protective and Immunomodulatory Functions of Exogenous B Cells in Experimental Hyperoxic Lung Injury.Anesthesia and analgesia · 2026Article
- Single-cell analysis of B cell dysregulation in pediatric sepsis stratified by disease severity.Scientific reports · 2025Observational
- Article
- The progress of organ protection mechanisms in sepsis.Frontiers in immunology · 2025Review
- Adaptation of SARS-CoV-2 to ACE2Journal of virology · 2024Article
- Genetic and immune determinants ofProceedings of the National Academy of Sciences of the United States of America · 2023Article
- Automated, high-throughput quantification of EGFP-expressing neutrophils in zebrafish by machine learning and a highly-parallelized microscope.bioRxiv : the preprint server for biology · 2023Article
- Genetic and immune determinants ofbioRxiv : the preprint server for biology · 2023Article
- Article
- Untargeted metabolomic profiling of sepsis-induced cardiac dysfunction.Frontiers in endocrinology · 2023Article
- Article
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Authors and funding
19 authors at 3 institutions in 2 countries.
Funding
Abstract
Sepsis is a life-threatening condition characterized by uncontrolled systemic inflammation and coagulation, leading to multiorgan failure. Therapeutic options to prevent sepsis-associated immunopathology remain scarce. Here, we established a mouse model of long-lasting disease tolerance during severe sepsis, manifested by diminished immunothrombosis and organ damage in spite of a high pathogen burden. We found that both neutrophils and B cells emerged as key regulators of tissue integrity. Enduring changes in the transcriptional profile of neutrophils include upregulated Cxcr4 expression in protected, tolerant hosts. Neutrophil Cxcr4 upregulation required the presence of B cells, suggesting that B cells promoted disease tolerance by improving tissue damage control via the suppression of neutrophils' tissue-damaging properties. Finally, therapeutic administration of a Cxcr4 agonist successfully promoted tissue damage control and prevented liver damage during sepsis. Our findings highlight the importance of a critical B-cell/neutrophil interaction during sepsis and establish neutrophil Cxcr4 activation as a potential means to promote disease tolerance during sepsis.
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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.