scholarly journals The Role of Formyl Peptide Receptors in Neurological Diseases via Regulating Inflammation

2021 ◽  
Vol 15 ◽  
Author(s):  
Jiahui Zhu ◽  
Lingfei Li ◽  
Jiao Ding ◽  
Jinyu Huang ◽  
Anwen Shao ◽  
...  
Keyword(s):  
Inflammatory Responses ◽  
Neurological Diseases ◽  
Cell Types ◽  
Dual Function ◽  
Peptide Receptors ◽  
Regulatory Pathways ◽  
Formyl Peptide Receptors ◽  
Neurogenic Tumors ◽  
Formyl Peptide

Formyl peptide receptors (FPRs) are a group of G protein-coupled cell surface receptors that play important roles in host defense and inflammation. Owing to the ubiquitous expression of FPRs throughout different cell types and since they interact with structurally diverse chemotactic agonists, they have a dual function in inflammatory processes, depending on binding with different ligands so that accelerate or inhibit key intracellular kinase-based regulatory pathways. Neuroinflammation is closely associated with the pathogenesis of neurodegenerative diseases, neurogenic tumors and cerebrovascular diseases. From recent studies, it is clear that FPRs are important biomarkers for neurological diseases as they regulate inflammatory responses by monitoring glial activation, accelerating neural differentiation, regulating angiogenesis, and controlling blood brain barrier (BBB) permeability, thereby affecting neurological disease progression. Given the complex mechanisms of neurological diseases and the difficulty of healing, we are eager to find new and effective therapeutic targets. Here, we review recent research about various mechanisms of the effects generated after FPR binding to different ligands, role of FPRs in neuroinflammation as well as the development and prognosis of neurological diseases. We summarize that the FPR family has dual inflammatory functional properties in central nervous system. Emphasizing that FPR2 acts as a key molecule that mediates the active resolution of inflammation, which binds with corresponding receptors to reduce the expression and activation of pro-inflammatory composition, govern the transport of immune cells to inflammatory tissues, and restore the integrity of the BBB. Concurrently, FPR1 is essentially related to angiogenesis, cell proliferation and neurogenesis. Thus, treatment with FPRs-modulation may be effective for neurological diseases.

scholarly journals The Role of Formyl Peptide Receptors in Permanent and Low-Grade Inflammation: Helicobacter pylori Infection as a Model

2021 ◽  
Vol 22 (7) ◽  
pp. 3706
Author(s):  
Paola Cuomo ◽  
Marina Papaianni ◽  
Rosanna Capparelli ◽  
Chiara Medaglia
Keyword(s):  
Helicobacter Pylori ◽  
Inflammatory Responses ◽  
Inflammatory Diseases ◽  
Formyl Peptide Receptor ◽  
Surface Pattern ◽  
Low Grade ◽  
Peptide Receptors ◽  
Formyl Peptide Receptors ◽  
Formyl Peptide

Formyl peptide receptors (FPRs) are cell surface pattern recognition receptors (PRRs), belonging to the chemoattractant G protein-coupled receptors (GPCRs) family. They play a key role in the innate immune system, regulating both the initiation and the resolution of the inflammatory response. FPRs were originally identified as receptors with high binding affinity for bacteria or mitochondria N-formylated peptides. However, they can also bind a variety of structurally different ligands. Among FPRs, formyl peptide receptor-like 1 (FPRL1) is the most versatile, recognizing N-formyl peptides, non-formylated peptides, and synthetic molecules. In addition, according to the ligand nature, FPRL1 can mediate either pro- or anti-inflammatory responses. Hp(2-20), a Helicobacter pylori-derived, non-formylated peptide, is a potent FPRL1 agonist, participating in Helicobacter pylori-induced gastric inflammation, thus contributing to the related site or not-site specific diseases. The aim of this review is to provide insights into the role of FPRs in H. pylori-associated chronic inflammation, which suggests this receptor as potential target to mitigate both microbial and sterile inflammatory diseases.

The Role of Formyl Peptide Receptors in Microbial Infection and Inflammation

2003 ◽  
Vol 2 (1) ◽  
pp. 83-93 ◽  
Author(s):  
Yingying Le ◽  
Ronghua Sun ◽  
Guoguang Ying ◽  
Pablo Iribarren ◽  
Ji Wang
Keyword(s):  
Microbial Infection ◽  
Peptide Receptors ◽  
Formyl Peptide Receptors ◽  
Formyl Peptide ◽  
Infection And Inflammation

The Role of Formyl Peptide Receptors for Immunomodulatory Activities of Antimicrobial Peptides and Peptidomimetics

2018 ◽  
Vol 24 (10) ◽  
pp. 1100-1120 ◽  
Author(s):  
Sarah Line Skovbakke ◽  
Andre Holdfeldt ◽  
Huamei Forsman ◽  
Johan Bylund ◽  
Henrik Franzyk
Keyword(s):  
Antimicrobial Peptides ◽  
Therapeutic Potential ◽  
Biological Activities ◽  
Chemical Properties ◽  
Immunomodulatory Activity ◽  
Peptide Receptors ◽  
Formyl Peptide Receptors ◽  
Formyl Peptide ◽  
Natural And Synthetic

In recent years, the therapeutic potential of antimicrobial peptides (AMPs) as immunomodulators has become generally accepted. Nevertheless, only very few AMP-based compounds have progressed into clinical trials. This paradox may be explained by the fact, that some of the intrinsic properties of natural peptides, such as proteolytic and oxidative instability, render them inconvenient as therapeutics. Therefore, substantial research efforts have been dedicated to mimic the physico-chemical properties as well as biological activities of AMPs by designing and identifying more stable peptidomimetics displaying analogous immunomodulatory activity profiles. Neutrophils play key roles in host defense as major effector cells in clearance of pathogens by phagocytosis and by regulating other processes of innate immunity as well as by promoting resolution of inflammation. Several aspects of these effects are correlated to their expression of formyl peptide receptors (FPRs) that have been shown to be targets of both natural and synthetic antimicrobial peptides. In the present review recent findings highlighting the role of FPRs in mediating immunomodulatory activities of natural and synthetic AMPs as well as of stabilized peptidomimetics are discussed, and prospects for future development of immunomodulatory therapeutics are presented.

scholarly journals Annexin A1 Released in Extracellular Vesicles by Pancreatic Cancer Cells Activates Components of the Tumor Microenvironment, through Interaction with the Formyl-Peptide Receptors

Cells ◽  
2020 ◽  
Vol 9 (12) ◽  
pp. 2719
Author(s):  
Nunzia Novizio ◽  
Raffaella Belvedere ◽  
Emanuela Pessolano ◽  
Alessandra Tosco ◽  
Amalia Porta ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Tumor Microenvironment ◽  
Extracellular Vesicles ◽  
Soluble Form ◽  
Annexin A1 ◽  
Peptide Receptors ◽  
Formyl Peptide Receptors ◽  
Pancreatic Cancer Cells ◽  
Formyl Peptide

Pancreatic cancer (PC) is one of the most aggressive cancers in the world. Several extracellular factors are involved in its development and metastasis to distant organs. In PC, the protein Annexin A1 (ANXA1) appears to be overexpressed and may be identified as an oncogenic factor, also because it is a component in tumor-deriving extracellular vesicles (EVs). Indeed, these microvesicles are known to nourish the tumor microenvironment. Once we evaluated the autocrine role of ANXA1-containing EVs on PC MIA PaCa-2 cells and their pro-angiogenic action, we investigated the ANXA1 paracrine effect on stromal cells like fibroblasts and endothelial ones. Concerning the analysis of fibroblasts, cell migration/invasion, cytoskeleton remodeling, and the different expression of specific protein markers, all features of the cell switching into myofibroblasts, were assessed after administration of wild type more than ANXA1 Knock-Out EVs. Interestingly, we demonstrated a mechanism by which the ANXA1-EVs complex can stimulate the activation of formyl peptide receptors (FPRs), triggering mesenchymal switches and cell motility on both fibroblasts and endothelial cells. Therefore, we highlighted the importance of ANXA1/EVs-FPR axes in PC progression as a vehicle of intercommunication tumor cells-stroma, suggesting a specific potential prognostic/diagnostic role of ANXA1, whether in soluble form or even if EVs are captured in PC.

Role of Formyl-Peptide Receptors in Chronic Rhinosinusitis

2010 ◽  
Vol 143 (2_suppl) ◽  
pp. P137-P137
Author(s):  
Amato de Paulis ◽  
Nella Prevete ◽  
Gianni Marone ◽  
Massimo Dellepiane ◽  
Renzo Mora
Keyword(s):  
Chronic Rhinosinusitis ◽  
Peptide Receptors ◽  
Formyl Peptide Receptors ◽  
Formyl Peptide

Biological Role of the N-Formyl Peptide Receptors

2006 ◽  
Vol 28 (1) ◽  
pp. 103-127 ◽  
Author(s):  
M.A. Panaro ◽  
A. Acquafredda ◽  
M. Sisto ◽  
S. Lisi ◽  
A.B. Maffione ◽  
...  
Keyword(s):  
Biological Role ◽  
Peptide Receptors ◽  
Formyl Peptide Receptors ◽  
Formyl Peptide

Emerging contributions of formyl peptide receptors to neurodegenerative diseases

2021 ◽  
Vol 0 (0) ◽  
Author(s):  
Lukas Busch ◽  
Stefan Vieten ◽  
Susan Brödel ◽  
Kristina Endres ◽  
Bernd Bufe
Keyword(s):  
Neurodegenerative Diseases ◽  
Inflammatory Responses ◽  
Central Element ◽  
Peptide Receptors ◽  
Lipoxin A4 ◽  
Formyl Peptide Receptors ◽  
Formyl Peptide ◽  
Dependent Signal ◽  
Dependent Cell ◽  
Novel Therapeutic Strategies

Abstract Inflammation is a central element of many neurodegenerative diseases. Formyl peptide receptors (FPRs) can trigger several receptor-dependent signal transduction pathways that play a key role in neuroinflammation and neurodegeneration. They are chemotactic receptors that help to regulate pro- and anti-inflammatory responses in most mammals. FPRs are primarily expressed in the immune and nervous systems where they interact with a complex pattern of pathogen-derived and host-endogenous molecules. Mounting evidence points towards a contribution of FPRs – via neuropathological ligands such as Amyloid beta, and neuroprotective ligands such as Humanin, Lipoxin A4, and Annexin A1 – to multiple pathological aspects of neurodegenerative diseases. In this review, we aim to summarize the interplay of FPRs with neuropathological and neuroprotective ligands. Next, we depict their capability to trigger a number of ligand-dependent cell signaling pathways and their potential to interact with additional intracellular cofactors. Moreover, we highlight first studies, demonstrating that a pharmacological inhibition of FPRs helps to ameliorate neuroinflammation, which may pave the way towards novel therapeutic strategies.

Role of Formyl Peptide Receptors in Gastrointestinal Healing

2018 ◽  
Vol 24 (18) ◽  
pp. 1966-1971 ◽  
Author(s):  
N. Prevete ◽  
A. de Paulis ◽  
D. Sgambato ◽  
R.M. Melillo ◽  
G. D`Argenio ◽  
...  
Keyword(s):  
Gi Tract ◽  
Peptide Receptors ◽  
Epithelial Repair ◽  
Formyl Peptide Receptors ◽  
Treatment Regimens ◽  
Injured Tissue ◽  
Formyl Peptide ◽  
New Treatment ◽  
Gi Mucosa

The wound healing and the barrier restoration of the gastrointestinal (GI) mucosa must be continuously ensured to allow homeostasis of the gastrointestinal tract and of all the surrounding tissues. Several lines of the evidence report a key role of innate immunity, and in particular of Pattern Recognition Receptors (PRRs), in controlling the homeostasis of GI tract by sensing commensal and pathogen bacteria, activating the immune response and regulating epithelial repair, thus guaranteeing the morphological and functional recovery of the injured tissue. We will discuss the role of a particular class of PRRs - the Formyl Peptide Receptors - in the homeostasis of GI mucosa. We here report the results of studies that strongly suggest the possibility that the activation of FPRs is crucial in the maintenance of homeostasis of the GI tract and provide indications of the potential clinical relevance of new treatment regimens involving FPR modulation for several GI disorders.

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