ArticleOncotarget2016
Exogenous carbon monoxide inhibits neutrophil infiltration in LPS-induced sepsis by interfering with FPR1 via p38 MAPK but not GRK2.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 35 citations in OpenAlex.
- Harnessing gasotransmitters for orthopaedic infection therapy: Mechanisms and advanced delivery platforms.Bioactive materials · 2027Review
- Wearable and battery-free wound dressing system for wireless and early sepsis diagnosis.Bioengineering & translational medicine · 2023Article
- Skewing cPLAScience signaling · 2023Article
- Cargo-free particles divert neutrophil-platelet aggregates to reduce thromboinflammation.Nature communications · 2023Article
- Review
- Bistable Mathematical Model of Neutrophil Migratory Patterns After LPS-Induced Epigenetic Reprogramming.Frontiers in genetics · 2021Article
- Pulmonary Inflammation and KRAS Mutation in Lung Cancer.Advances in experimental medicine and biology · 2021Article
- Neutrophil chemoattractant receptors in health and disease: double-edged swords.Cellular & molecular immunology · 2020Review
- Carbon monoxide in intensive care medicine-time to start the therapeutic application?!Intensive care medicine experimental · 2020Review
- The Neutrophil: Constant Defender and First Responder.Frontiers in immunology · 2020Review
- Hepatoprotective effects of vicenin-2 and scolymoside through the modulation of inflammatory pathways.Journal of natural medicines · 2020Article
- Carbon monoxide releasing molecule‑2 (CORM‑2)‑liberated CO ameliorates acute pancreatitis.Molecular medicine reports · 2019Article
- Luteolin Partially Inhibits LFA-1 Expression in Neutrophils Through the ERK Pathway.Inflammation · 2019Article
- The frequency of ANCA-associated vasculitis in a national database of hospitalized patients in China.Arthritis research & therapy · 2018Article
- FPR1 mediates the tumorigenicity of human cervical cancer cells.Cancer management and research · 2018Article
- Adenosine effectively restores endotoxin-induced inhibition of human neutrophil chemotaxis via A1 receptor-p38 pathway.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2017Article
- Pro-Resolving Molecules-New Approaches to Treat Sepsis?International journal of molecular sciences · 2017Review
- Tuftsin prevents the negative immunoregulation of neuropilin-1highCD4+CD25+Regulatory T cells and improves survival rate in septic mice.Oncotarget · 2016Article
- Severe COVID-19: NLRP3 Inflammasome Dysregulated.Frontiers in immunologyReview
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Excessive neutrophil infiltration in vital organs is life-threatening to patients who suffer from sepsis. We identified a critical role of exogenous carbon monoxide (CO) in the inhibition of neutrophil infiltration during lipopolysaccharide (LPS)-induced sepsis. CO delivered from carbon monoxide-releasing molecule 2 (CORM-2) dramatically increased the survival rate of C57BL/6 mice subjected to LPS in vivo. CORM-2 significantly suppressed neutrophil infiltration in liver and lung as well as markers of inflammatory responses. Affymetrix GeneChip array analysis revealed that the increased expression of chemoattractant receptor formyl peptide receptor 1 (FPR1) may contribute to the excessive neutrophil infiltration. The under agarose migration assay demonstrated that LPS stimulation promoted migration to the ligand of FPR1, N-Formyl-Met-Leu-Phe (fMLP) but that CORM-2 treatment inhibited this promotion. Further studies demonstrated that CORM-2 internalized FPR1 by inhibiting p38 mitogen-activated protein kinase (MAPK) but not G protein-coupled receptor kinase 2 (GRK2), which may explain the inhibitory effect of CORM-2 on LPS-stimulated neutrophils. In summary, our study demonstrates that exogenous CO inhibits sepsis-induced neutrophil infiltration by interfering with FPR1 via p38 MAPK but not GRK2.
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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.