ArticlePloS one2014
Deficiency of formyl peptide receptor 1 and 2 is associated with increased inflammation and enhanced liver injury after LPS-stimulation.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 38 citations in OpenAlex.
- Genetic deletion of Alx/Fpr2 differentially regulates pulmonary inflammation in the absence and presence of acute lung injury.ImmunoHorizons · 2025Article
- Contribution of Sex Differences to the Development of Cardiovascular Disease in Metabolic-Associated Steatotic Liver Disease (MASLD).International journal of translational medicine (Basel, Switzerland) · 2024Article
- Article
- Phospholipids impact the protective effects of HDL-mimetic nanodiscs against lipopolysaccharide-induced inflammation.Nanomedicine (London, England) · 2023Article
- Article
- Formyl peptide receptor 2 is an emerging modulator of inflammation in the liver.Experimental & molecular medicine · 2023Review
- Rs867228 in FPR1 accelerates the manifestation of luminal B breast cancer.Oncoimmunology · 2023Article
- Formyl peptide receptor-1 (FPR1) represses intestinal oncogenesis.Oncoimmunology · 2023Article
- Formylpeptide receptor 2: Nomenclature, structure, signalling and translational perspectives: IUPHAR review 35.British journal of pharmacology · 2022Review
- Formyl peptide receptor 2 determines sex-specific differences in the progression of nonalcoholic fatty liver disease and steatohepatitis.Nature communications · 2022Article
- 6-Shogaol Mitigates Sepsis-Associated Hepatic Injury through Transcriptional Regulation.Nutrients · 2021Article
- Activation of formyl peptide receptor 1 elicits therapeutic effects against collagen-induced arthritis.Journal of cellular and molecular medicine · 2021Article
- Article
- A major genetic accelerator of cancer diagnosis: rs867228 in FPR1.Oncoimmunology · 2021Article
- Article
- Fpr2/CXCL1/2 Controls Rapid Neutrophil Infiltration to InhibitFrontiers in immunology · 2021Article
- The formyl peptide receptor agonist Ac2-26 alleviates neuroinflammation in a mouse model of pneumococcal meningitis.Journal of neuroinflammation · 2020Article
- Inhibition of formyl peptide receptor 1 activity suppresses tumorigenicityAnnals of translational medicine · 2020Article
- Formyl peptide receptor 2 regulates monocyte recruitment to promote intestinal mucosal wound repair.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- MicroRNA-149* suppresses hepatic inflammatory response through antagonizing STAT3 signaling pathway.Oncotarget · 2017Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionFormyl peptide-receptor 1 and 2 (FPR1 and FPR2) in mice were identified as receptors with contrary affinity for the PAMP fMLF. Formyl-methionyl-leucyl-phenylalanine is either part of the bacterial membrane and is secreted by the mitochondria of eukaryotic ceslls during apoptosis. Furthermore FPR1 and 2 are described as highly relevant factors for the chemotaxis of immune cells. Their role during the acute liver injury has not been investigated yet. MATERIALS AND
methodsConstitutive knockout mice for FPR1 (mFPR1-/-), FPR2 (mFPR2-/-) and wild type (WT) mice were challenged with LPS i.p. for 3 h and 6 h. Liver and serum were sampled for further analysis.
resultsLiver transaminases were elevated in all mice 3 h and 6 h post LPS stimulation. Gene expression analysis displayed a reduced expression of the pro-inflammatory cytokines IL-6 and CXCL1 after 3 h in the mFPR1-/- compared to wild type and mFPR2-/- mice. After 6 h, IL-6, TNF-α and CXCL1 were significantly higher in mice lacking mFPR1 or 2. Consistent to these findings the numbers of CD11b+ and Ly6G+ immune cells were altered in the livers. The analysis of TLR2 and TLR4 revealed time and genotype specific changes in theirs gene expression. Additionally, the liver in mFPR1- and mFPR2-deficient mice seem to be more susceptible to apoptosis by showing a significant higher number of TUNEL+-cells in the liver than WT-mice and displayed less Ki67-positive nuclei in the liver.
conclusionThe results suggest a prominent role of FPRs in the regulation of the hepatic inflammatory response after LPS induced liver injury. Deletion of mFPR1 or mFPR2 leads to deregulation of the inflammatory response compared to WT mice, associated with more severe liver injury represented by higher levels of transaminases, apoptotic cells and a reduced regenerative capacity.
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