ArticleProceedings of the National Academy of Sciences of the United States of America2014
Nonredundant protective properties of FPR2/ALX in polymicrobial murine sepsis.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.
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Who cites it
68 citing papers in PubMed, 117 citations in OpenAlex.
- FPR2 deficiency alleviates LPS-induced depressive-like behaviors in mice by suppressing the microglial CSF1/NLRP3 inflammasome pathway.Journal of neuroinflammation · 2026Article
- G protein-coupled receptors and inflammation resolution signaling networks in the heart: Pharmacology and potential for innovative therapeutics.Pharmacological reviews · 2026Review
- Research Progress of Annexin A1 and Its Derived Peptides in the Diagnosis and Treatment of Circulatory Diseases.Immunity, inflammation and disease · 2025Review
- Resolution Pharmacology: State-of-the-art and therapeutic landscape.Pharmacological reviews · 2025Review
- Genetic deletion of Alx/Fpr2 differentially regulates pulmonary inflammation in the absence and presence of acute lung injury.ImmunoHorizons · 2025Article
- Formyl peptide receptor 2: a potential therapeutic target for inflammation-related diseases.Pharmacological reports : PR · 2025Review
- 17(R)-Resolvin D1 protects against sickle cell-related inflammatory cardiomyopathy in humanized mice.Blood · 2025Article
- Role of FPR2 antagonism in alleviating social isolation-induced depression and protecting blood-brain barrier integrity.Journal of neuroinflammation · 2025Article
- eIF3a function in immunity and protection against severe sepsis by regulating B cell quantity and function through mActa pharmaceutica Sinica. B · 2025Article
- Targeting formyl peptide receptor 2 to suppress neuroinflammation in neuromyelitis optica spectrum disorder.Theranostics · 2025Article
- Stimulation of the Pro-Resolving Receptor Fpr2 Reverses Inflammatory Microglial Activity by Suppressing NFκB Activity.International journal of molecular sciences · 2023Article
- Maresin1 prevents sepsis-induced acute liver injury by suppressing NF-κB/Stat3/MAPK pathways, mitigating inflammation.Heliyon · 2023Article
- Transcriptome sequencing and experiments reveal the effect of formyl peptide receptor 2 on liver homeostasis.World journal of gastroenterology · 2023Article
- Developmental and homeostatic signaling transmitted by the G-protein coupled receptor FPR2.International immunopharmacology · 2023Review
- Article
- Identification of PIK3CG as a hub in septic myocardial injury using network pharmacology and weighted gene co-expression network analysis.Bioengineering & translational medicine · 2023Article
- Formylpeptide receptor 2: Nomenclature, structure, signalling and translational perspectives: IUPHAR review 35.British journal of pharmacology · 2022Review
- Interferon-β regulates proresolving lipids to promote the resolution of acute airway inflammation.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Impact of High-Molecular-Weight Hyaluronic Acid on Gene Expression in Rabbit Achilles Tenocytes In Vitro.International journal of molecular sciences · 2022Article
- Article
8 more citing papers are in PubMed but not listed here.
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Authors and funding
9 authors at 4 institutions in 3 countries.
Funding
Abstract
Sepsis is characterized by overlapping phases of excessive inflammation temporally aligned with an immunosuppressed state, defining a complex clinical scenario that explains the lack of successful therapeutic options. Here we tested whether the formyl-peptide receptor 2/3 (Fpr2/3)--ortholog to human FPR2/ALX (receptor for lipoxin A4)--exerted regulatory and organ-protective functions in experimental sepsis. Coecal ligature and puncture was performed to obtain nonlethal polymicrobial sepsis, with animals receiving antibiotics and analgesics. Clinical symptoms, temperature, and heart function were monitored up to 24 h. Peritoneal lavage and plasma samples were analyzed for proinflammatory and proresolving markers of inflammation and organ dysfunction. Compared with wild-type mice, Fpr2/3(-/-) animals exhibited exacerbation of disease severity, including hypothermia and cardiac dysfunction. This scenario was paralleled by higher levels of cytokines [CXCL1 (CXC receptor ligand 1), CCL2 (CC receptor ligand 2), and TNFα] as quantified in cell-free biological fluids. Reduced monocyte recruitment in peritoneal lavages of Fpr2/3(-/-) animals was reflected by a higher granulocyte/monocyte ratio. Monitoring Fpr2/3(-/-) gene promoter activity with a GFP proxy marker revealed an over threefold increase in granulocyte and monocyte signals at 24 h post-coecal ligature and puncture, a response mediated by TNFα. Treatment with a receptor peptido-agonist conferred protection against myocardial dysfunction in wild-type, but not Fpr2/3(-/-), animals. Therefore, coordinated physio-pharmacological analyses indicate nonredundant modulatory functions for Fpr2/3 in experimental sepsis, opening new opportunities to manipulate the host response for therapeutic development.
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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.