scholarly journals Lipoxin Receptors

2007 ◽  
Vol 7 ◽  
pp. 1393-1412 ◽  
Author(s):  
Mario Romano ◽  
Irene Recchia ◽  
Antonio Recchiuti
Keyword(s):  
Current Knowledge ◽  
Cell Types ◽  
Formyl Peptide Receptor ◽  
Peptide Receptor ◽  
The Family ◽  
Pathophysiological Role ◽  
Formyl Peptide ◽  
Anti Inflammatory ◽  
Main Components

Lipoxins (LXs) represent a class of arachidonic acid (AA) metabolites that carry potent immunoregulatory and anti-inflammatory properties, LXA4and LXB4being the main components of this series. LXs are generated by cooperation between 5-lipoxygenase (LO) and 12- or 15-LO during cell-cell interactions or by single cell types. LX epimers at carbon 15, the 15-epi-LXs, are formed by aspirin-acetylated cyclooxygenase-2 (COX-2) in cooperation with 5-LO. 15-epi-LXA4is also termed aspirin-triggered LX (ATL).In vivostudies with stable LX and ATL analogs have established that these eicosanoids possess potent anti-inflammatory activities. A LXA4receptor has been cloned. It belongs to the family of chemotactic receptors and clusters with formyl peptide receptors on chromosome 19. Therefore, it was initially denominated formyl peptide receptor like 1 (FPRL1). This receptor binds with high affinity and stereoselectivity LXA4and ATL. It also recognizes a variety of peptides, synthetic, endogenously generated, or disease associated, but with lower affinity compared to LXA4. For this reason, this receptor has been renamed ALX. This review summarizes the current knowledge on ALX expression, signaling, and potential pathophysiological role. The involvement of additional recognition sites in LX bioactions is also discussed.

scholarly journals The N-Formyl Peptide Receptor 2 (FPR2) Agonist MR-39 Improves Ex Vivo and In Vivo Amyloid Beta (1–42)-Induced Neuroinflammation in Mouse Models of Alzheimer’s Disease

2021 ◽  
Author(s):  
Ewa Trojan ◽  
Kinga Tylek ◽  
Nicole Schröder ◽  
Iris Kahl ◽  
Lars-Ove Brandenburg ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Inflammatory Cytokines ◽  
Ex Vivo ◽  
Neuronal Loss ◽  
Formyl Peptide Receptor ◽  
Peptide Receptor ◽  
Formyl Peptide ◽  
Anti Inflammatory

Abstract The major histopathological hallmarks of Alzheimer’s disease (AD) include β-amyloid (Aβ) plaques, neurofibrillary tangles, and neuronal loss. Aβ 1–42 (Aβ1-42) has been shown to induce neurotoxicity and secretion of proinflammatory mediators that potentiate neurotoxicity. Proinflammatory and neurotoxic activities of Aβ1-42 were shown to be mediated by interactions with several cell surface receptors, including the chemotactic G protein-coupled N-formyl peptide receptor 2 (FPR2). The present study investigated the impact of a new FPR2 agonist, MR-39, on the neuroinflammatory response in ex vivo and in vivo models of AD. To address this question, organotypic hippocampal cultures from wild-type (WT) and FPR2-deficient mice (knockout, KO, FPR2−/−) were treated with fibrillary Aβ1-42, and the effect of the new FPR2 agonist MR-39 on the release of pro- and anti-inflammatory cytokines was assessed. Similarly, APP/PS1 double-transgenic AD mice were treated for 20 weeks with MR-39, and immunohistological staining was performed to assess neuronal loss, gliosis, and Aβ load in the hippocampus and cortex. The data indicated that MR-39 was able to reduce the Aβ1-42-induced release of proinflammatory cytokines and to improve the release of anti-inflammatory cytokines in mouse hippocampal organotypic cultures. The observed effect was apparently related to the inhibition of the MyD88/TRAF6/NFкB signaling pathway and a decrease in NLRP3 inflammasome activation. Administration of MR-39 to APP/PS1 mice improved neuronal survival and decreased microglial cell density and plaque load.These results suggest that FPR2 may be a promising target for alleviating the inflammatory process associated with AD and that MR-39 may be a useful therapeutic agent for AD.

Dual modulation of formyl peptide receptor 2 by aspirin‐triggered lipoxin contributes to its anti‐inflammatory activity

2020 ◽  
Vol 34 (5) ◽  
pp. 6920-6933 ◽  
Author(s):  
Yunjun Ge ◽  
Shuo Zhang ◽  
Junlin Wang ◽  
Fangbo Xia ◽  
Jian‐Bo Wan ◽  
...  
Keyword(s):  
Inflammatory Activity ◽  
Formyl Peptide Receptor ◽  
Peptide Receptor ◽  
Formyl Peptide ◽  
Anti Inflammatory

Design and characterization of a cleavage-resistant Annexin A1 mutant to control inflammation in the microvasculature

Blood ◽  
2010 ◽  
Vol 116 (20) ◽  
pp. 4288-4296 ◽  
Author(s):  
Magali Pederzoli-Ribeil ◽  
Francesco Maione ◽  
Dianne Cooper ◽  
Adam Al-Kashi ◽  
Jesmond Dalli ◽  
...  
Keyword(s):  
Polymorphonuclear Leukocytes ◽  
Early Stage ◽  
Leukocyte Adhesion ◽  
Formyl Peptide Receptor ◽  
Annexin A1 ◽  
Formyl Peptide ◽  
Anti Inflammatory ◽  
Human Polymorphonuclear Leukocytes

Abstract Human polymorphonuclear leukocytes adhesion to endothelial cells during the early stage of inflammation leads to cell surface externalization of Annexin A1 (AnxA1), an effector of endogenous anti-inflammation. The antiadhesive properties of AnxA1 become operative to finely tune polymorphonuclear leukocytes transmigration to the site of inflammation. Membrane bound proteinase 3 (PR3) plays a key role in this microenvironment by cleaving the N terminus bioactive domain of AnxA1. In the present study, we generated a PR3-resistant human recombinant AnxA1—named superAnxA1 (SAnxA1)—and tested its in vitro and in vivo properties in comparison to the parental protein. SAnxA1 bound and activated formyl peptide receptor 2 in a similar way as the parental protein, while showing a resistance to cleavage by recombinant PR3. SAnxA1 retained anti-inflammatory activities in the murine inflamed microcirculation (leukocyte adhesion being the readout) and in skin trafficking model. When longer-lasting models of inflammation were applied, SAnxA1 displayed stronger anti-inflammatory effect over time compared with the parental protein. Together these results indicate that AnxA1 cleavage is an important process during neutrophilic inflammation and that controlling the balance between AnxA1/PR3 activities might represent a promising avenue for the discovery of novel therapeutic approaches.

scholarly journals Evidence for an Anti-Inflammatory Loop Centered on Polymorphonuclear Leukocyte Formyl Peptide Receptor 2/Lipoxin A4Receptor and Operative in the Inflamed Microvasculature

2011 ◽  
Vol 186 (8) ◽  
pp. 4905-4914 ◽  
Author(s):  
Vincenzo Brancaleone ◽  
Jesmond Dalli ◽  
Stefania Bena ◽  
Roderick J. Flower ◽  
Giuseppe Cirino ◽  
...  
Keyword(s):  
Polymorphonuclear Leukocyte ◽  
Formyl Peptide Receptor ◽  
Peptide Receptor ◽  
Formyl Peptide ◽  
Anti Inflammatory

scholarly journals Staphylococcal superantigen-like protein 13 activates neutrophils via Formyl Peptide Receptor 2

2018 ◽  
Author(s):  
Yuxi Zhao ◽  
Kok P. M. van Kessel ◽  
Carla J. C. de Haas ◽  
Malbert R. C. Rogers ◽  
Jos A. G. van Strijp ◽  
...  
Keyword(s):  
Immune Evasion ◽  
Innate Immune ◽  
Formyl Peptide Receptor ◽  
Immune Functions ◽  
Peptide Receptor ◽  
Major Virulence Factor ◽  
Formyl Peptide ◽  
High Degree ◽  
Strong Activator

AbstractStaphylococcal Superantigen-Like (SSL) proteins, one of major virulence factor families produced byStaphylococcus aureus, were previously demonstrated to be immune evasion molecules that interfere with a variety of innate immune defenses. However, in contrast to these characterized SSLs, that inhibit immune functions, we show that SSL13 is a strong activator of neutrophils via the formyl-peptide receptor 2 (FPR2). Moreover, our data show that SSL13 acts as a chemoattractant, induces degranulation and oxidative burst in neutrophils. As with many other staphylococcal immune evasion proteins, SSL13 shows a high degree of human specificity. SSL13 is not able to efficiently activate mouse neutrophils, hamperingin vivoexperiments.In conclusion, SSL13 is a neutrophil chemoattractant and activator that acts via the FPR2. Therefore, SSL13 is a unique SSL member that does not belong to the immune evasion class, but is a pathogen alarming molecule.

scholarly journals A New Staphylococcal Anti-Inflammatory Protein That Antagonizes the Formyl Peptide Receptor-Like 1

2006 ◽  
Vol 177 (11) ◽  
pp. 8017-8026 ◽  
Author(s):  
Cristina Prat ◽  
Jovanka Bestebroer ◽  
Carla J. C. de Haas ◽  
Jos A. G. van Strijp ◽  
Kok P. M. van Kessel
Keyword(s):  
Formyl Peptide Receptor ◽  
Peptide Receptor ◽  
Inflammatory Protein ◽  
Formyl Peptide ◽  
Anti Inflammatory

scholarly journals Anti-Inflammatory Role of the Murine Formyl-Peptide Receptor 2: Ligand-Specific Effects on Leukocyte Responses and Experimental Inflammation

2010 ◽  
Vol 184 (5) ◽  
pp. 2611-2619 ◽  
Author(s):  
Neil Dufton ◽  
Robert Hannon ◽  
Vincenzo Brancaleone ◽  
Jesmond Dalli ◽  
Hetal B. Patel ◽  
...  
Keyword(s):  
Formyl Peptide Receptor ◽  
Peptide Receptor ◽  
Specific Effects ◽  
Formyl Peptide ◽  
Experimental Inflammation ◽  
Anti Inflammatory
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