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Journal articles on the topic "Specialized pro-resolution molecules"
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Chávez-Castillo, Mervin, Ángel Ortega, Lorena Cudris-Torres, Pablo Duran, Milagros Rojas, Alexander Manzano, Bermary Garrido, et al. "Specialized Pro-Resolving Lipid Mediators: The Future of Chronic Pain Therapy?" International Journal of Molecular Sciences 22, no. 19 (September 26, 2021): 10370. http://dx.doi.org/10.3390/ijms221910370.
Full textAbstract:
Chronic pain (CP) is a severe clinical entity with devastating physical and emotional consequences for patients, which can occur in a myriad of diseases. Often, conventional treatment approaches appear to be insufficient for its management. Moreover, considering the adverse effects of traditional analgesic treatments, specialized pro-resolving lipid mediators (SPMs) have emerged as a promising alternative for CP. These include various bioactive molecules such as resolvins, maresins, and protectins, derived from ω-3 polyunsaturated fatty acids (PUFAs); and lipoxins, produced from ω-6 PUFAs. Indeed, SPMs have been demonstrated to play a central role in the regulation and resolution of the inflammation associated with CP. Furthermore, these molecules can modulate neuroinflammation and thus inhibit central and peripheral sensitizations, as well as long-term potentiation, via immunomodulation and regulation of nociceptor activity and neuronal pathways. In this context, preclinical and clinical studies have evidenced that the use of SPMs is beneficial in CP-related disorders, including rheumatic diseases, migraine, neuropathies, and others. This review integrates current preclinical and clinical knowledge on the role of SPMs as a potential therapeutic tool for the management of patients with CP.
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Perniola, S., S. Alivernini, B. Tolusso, M. R. Gigante, M. Gessi, C. Di Mario, L. Petricca, et al. "AB0102 SPECIALIZED PRO-RESOLVING MEDIATOR RECEPTORS AS INFLAMMATORY RESOLUTION BIOMARKERS IN RHEUMATOID ARTHRITIS." Annals of the Rheumatic Diseases 79, Suppl 1 (June 2020): 1350.3–1350. http://dx.doi.org/10.1136/annrheumdis-2020-eular.6303.
Full textAbstract:
Background:The regulation of inflammation is a dynamic process involving several molecules as lipid mediators. The Specialized Pro-resolving Mediators (SPMs), such as Resolvin (RvD and RvE), Protectins, Maresins and Lipoxin A4 (LXA4), are bioactive metabolites of omega-3 and omega-6 fatty acids which drive inflammatory resolution phase and promote tissue repair. ERV, ALX/FPR2 and BLT1 are SPM receptors. Although in Rheumatoid Arthritis (RA) lipid mediators role within pathophysiology is under definition, studies on SPMs receptors role are still lacking in this disease.Objectives:Purpose of this study is to define ERV, ALX/FPR2 and BLT1 expression in blood derived leukocytes and synovial cells and to correlate it to disease activity to define SPM receptors ad inflammatory resolution biomarkers in RA patients.Methods:A cohort of 52 RA patients was enrolled in the study of which 40 with active disease (DAS28= 5,35 (5,18-6,40)) and 12 in sustained remission status (DAS28= 2,1 (1,83-2,42)). Each enrolled patient underwent peripheral blood (PB) drawing and 46 of them underwent US-guided synovial tissue (ST) biopsy. FACS gating strategy was used for PB and ST processing to evaluate percentage of positive cells and the mean fluorescence intensity (MFI) of ERV+, ALX/FPR2+and BLT1+in CD45+CD3+, CD45+CD19+for PB and ST, CD45+CD14+and neutrophils for PB only and CD45-CD90+, CD45+CD64+CD11b+macrophages (distinct in CD206+and CD206-subpopulations) for ST only. Each included ST was stained with haematoxylin/eosin and categorized by a pathologist, blinded to clinical characteristics, using the Krenn Score (KS) to assess ST inflammation degree. As control group, 11 undifferentiated peripheral inflammatory arthritis (UPIA) patients were enrolled in the study.Results:Considering the whole RA cohort, DAS28 inversely correlated with BLT1+positive cells on ST-derived CD45+(r= -0.48; p= 0.048), CD3+(r= -0.56; p= 0.019) and CD19+(r= -0.49; p= 0.042) cells, in contrast with CD90+(r= 0.50; p= 0.041) cells. Similarly, both DAS28 and KS inversely correlated with ALX/FPR2+positive cells in ST-derived CD45+(r= -0.42, p= 0.050 and r= -0,41, p= 0,046 respectively) cells. Evaluating the MFI levels of the SPM receptors along all RA stages (naïve-to-treatment, resistant-to-treatment, sustained remission) compared with UPIA control group, interestingly ST-derived CD45+cells of remission RA were depleted of ERV1 compared to naïve-to-treatment RA (p=0.04), despite comparable ST inflammation. Furthermore, highest ERV1 expression was found in ST-derived CD45+CD3+and CD45+CD19+cells in naïve-to-treatment RA compared with UPIA patients (p= 0,045 and p= 0,012 respectively). Moreover, the lowest BLT1 level was found in remission RA CD3+cells compared with UPIA and naïve-to-treatment RA patients (p= 0,008 and p= 0,023 respectively).Conclusion:SPM receptors expression seem to be tightly related to disease activity in the synovial tissue, suggesting an important involvement in the inflammatory process in RA patient.References:[1]Serhan CN. Nature, 2014.[2]Alivernini S, et al. Arthritis Res Ther 2016[3]Krenn V et al. Histopathology, 2006.Disclosure of Interests:Simone Perniola: None declared, Stefano Alivernini: None declared, Barbara Tolusso: None declared, Maria Rita Gigante: None declared, Marco Gessi: None declared, Clara Di Mario: None declared, Luca Petricca: None declared, Annunziata Capacci: None declared, Anna Laura Fedele: None declared, Gianfranco Ferraccioli: None declared, Elisa Gremese Speakers bureau: Abbvie, BMS, Celgene, Jannsen, Lilly, MSD, Novartis, Pfizer, Sandoz, UCB
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Hwang, Sung-Min, Gehoon Chung, Yong Ho Kim, and Chul-Kyu Park. "The Role of Maresins in Inflammatory Pain: Function of Macrophages in Wound Regeneration." International Journal of Molecular Sciences 20, no. 23 (November 21, 2019): 5849. http://dx.doi.org/10.3390/ijms20235849.
Full textAbstract:
Although acute inflammatory responses are host-protective and generally self-limited, unresolved and delayed resolution of acute inflammation can lead to further tissue damage and chronic inflammation. The mechanism of pain induction under inflammatory conditions has been studied extensively; however, the mechanism of pain resolution is not fully understood. The resolution of inflammation is a biosynthetically active process, involving specialized pro-resolving mediators (SPMs). In particular, maresins (MaRs) are synthesized from docosahexaenoic acid (DHA) by macrophages and have anti-inflammatory and pro-resolving capacities as well as tissue regenerating and pain-relieving properties. A new class of macrophage-derived molecules—MaR conjugates in tissue regeneration (MCTRs)—has been reported to regulate phagocytosis and the repair and regeneration of damaged tissue. Macrophages not only participate in the biosynthesis of SPMs, but also play an important role in phagocytosis. They exhibit different phenotypes categorized as proinflammatory M1-like phenotypes and anti-inflammatory M2 phenotypes that mediate both harmful and protective functions, respectively. However, the signaling mechanisms underlying macrophage functions and phenotypic changes have not yet been fully established. Recent studies report that MaRs help resolve inflammatory pain by enhancing macrophage phagocytosis and shifting cytokine release to the anti-inflammatory M2 phenotypes. Consequently, this review elucidated the characteristics of MaRs and macrophages, focusing on the potent action of MaRs to enhance the M2 macrophage phenotype profiles that possess the ability to alleviate inflammatory pain.
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Tylek, Kinga, Ewa Trojan, Magdalena Regulska, Enza Lacivita, Marcello Leopoldo, and Agnieszka Basta-Kaim. "Formyl peptide receptor 2, as an important target for ligands triggering the inflammatory response regulation: a link to brain pathology." Pharmacological Reports 73, no. 4 (June 8, 2021): 1004–19. http://dx.doi.org/10.1007/s43440-021-00271-x.
Full textAbstract:
AbstractFormyl peptide receptors (FPRs) belong to the family of seven-transmembrane G protein-coupled receptors. Among them, FPR2 is a low affinity receptor for N-formyl peptides and is considered the most promiscuous member of FPRs. FPR2 is able to recognize a broad variety of endogenous or exogenous ligands, ranging from lipid to proteins and peptides, including non-formylated peptides. Due to this property FPR2 has the ability to modulate both pro- and anti-inflammatory response, depending on the nature of the bound agonist and on the different recognition sites of the receptor. Thus, FPR2 takes part not only in the proinflammatory response but also in the resolution of inflammation (RoI) processes. Recent data have indicated that the malfunction of RoI may be the background for some central nervous system (CNS) disorders. Therefore, much interest is focused on endogenous molecules called specialized pro-resolving mediators (SPMs), as well as on new synthetic FPR2 agonists, which kick-start the resolution of inflammation (RoI) and modulate its course. Here, we shed some light on the general characteristics of the FPR family in humans and in the experimental animals. Moreover, we present a guide to understanding the “double faced” action of FPR2 activation in the context of immune-related diseases of the CNS.
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Trojan, Ewa, Natalia Bryniarska, Monika Leśkiewicz, Magdalena Regulska, Katarzyna Chamera, Magdalena Szuster-Głuszczak, Marcello Leopoldo, Enza Lacivita, and Agnieszka Basta-Kaim. "The Contribution of Formyl Peptide Receptor Dysfunction to the Course of Neuroinflammation: A Potential Role in the Brain Pathology." Current Neuropharmacology 18, no. 3 (February 14, 2020): 229–49. http://dx.doi.org/10.2174/1570159x17666191019170244.
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: Chronic inflammatory processes within the central nervous system (CNS) are in part responsible for the development of neurodegenerative and psychiatric diseases. These processes are associated with, among other things, the increased and disturbed activation of microglia and the elevated production of proinflammatory factors. Recent studies indicated that the disruption of the process of resolution of inflammation (RoI) may be the cause of CNS disorders. It is shown that the RoI is regulated by endogenous molecules called specialized pro-resolving mediators (SPMs), which interact with specific membrane receptors. Some SPMs activate formyl peptide receptors (FPRs), which belong to the family of seven-transmembrane G protein-coupled receptors. These receptors take part not only in the proinflammatory response but also in the resolution of the inflammation process. Therefore, the activation of FPRs might have complex consequences. : This review discusses the potential role of FPRs, and in particular the role of FPR2 subtype, in the brain under physiological and pathological conditions and their involvement in processes underlying neurodegenerative and psychiatric disorders as well as ischemia, the pathogenesis of which involves the dysfunction of inflammatory processes.
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Vassallo, Arlette, Alex J. Wood, Julien Subburayalu, Charlotte Summers, and Edwin R. Chilvers. "The counter-intuitive role of the neutrophil in the acute respiratory distress syndrome." British Medical Bulletin 131, no. 1 (September 2019): 43–55. http://dx.doi.org/10.1093/bmb/ldz024.
Full textAbstract:
Abstract Introduction Neutrophils are the primary effectors of the innate immune system but are profoundly histotoxic cells. The acute respiratory distress syndrome (ARDS) is considered to be a prime example of neutrophil-mediated tissue injury. Sources of data The information presented in this review is acquired from the published neutrophil cell biology literature and the longstanding interest of the senior authors in ARDS pathogenesis and clinical management. Areas of agreement Investigators in the field would agree that neutrophils accumulate in high abundance in the pulmonary microcirculation, lung interstitium and alveolar airspace of patients with ARDS. ARDS is also associated with systemic neutrophil priming and delayed neutrophil apoptosis and clearance of neutrophils from the lungs. In animal models, reducing circulating neutrophil numbers ameliorates lung injury. Areas of controversy Areas of uncertainty include how neutrophils get stuck in the narrow pulmonary capillary network—whether this reflects changes in the mechanical properties of primed neutrophils alone or additional cell adhesion molecules, the role of neutrophil sub-sets or polarization states including pro-angiogenic and low-density neutrophils, whether neutrophil extracellular trap (NET) formation is beneficial (through bacterial capture) or harmful and the potential for neutrophils to participate in inflammatory resolution. The latter may involve the generation of specialized pro-resolving molecules (SPMs) and MMP-9, which is required for adequate matrix processing. Growing points Different and possibly stable endotypes of ARDS are increasingly being recognized, yet the relative contribution of the neutrophil to these endotypes is uncertain. There is renewed and intense interest in understanding the complex ‘new biology’ of the neutrophil, specifically whether this cell might be a valid therapeutic target in ARDS and other neutrophil-driven diseases and developing understanding of ways to enhance the beneficial role of the neutrophil in the resolution phase of ARDS. Areas timely for developing research Aside from treatment of the precipitating causes of ARDS, and scrupulous fluid, infection and ventilation management, there are no pharmacological interventions for ARDS; this represents an urgent and unmet need. Therapies aimed at reducing overall neutrophil numbers risk secondary infection; hence better ways are needed to reverse the processes of neutrophil priming activation, hyper-secretion and delayed apoptosis while enhancing the pro-resolution functions of the neutrophil.
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Regidor, Pedro-Antonio, Anna Mueller, Manuela Sailer, Fernando Gonzalez Santos, Jose Miguel Rizo, and Fernando Moreno Egea. "Chronic Inflammation in PCOS: The Potential Benefits of Specialized Pro-Resolving Lipid Mediators (SPMs) in the Improvement of the Resolutive Response." International Journal of Molecular Sciences 22, no. 1 (December 31, 2020): 384. http://dx.doi.org/10.3390/ijms22010384.
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PCOS as the most common endocrine disorder of women in their reproductive age affects between 5–15% of the female population. Apart from its cardinal symptoms, like irregular and anovulatory cycles, hyperandrogenemia and a typical ultrasound feature of the ovary, obesity, and insulin resistance are often associated with the disease. Furthermore, PCOS represents a status of chronic inflammation with permanently elevated levels of inflammatory markers including IL-6 and IL-18, TNF-α, and CRP. Inflammation, as discovered only recently, consists of two processes occurring concomitantly: active initiation, involving “classical” mediators including prostaglandins and leukotrienes, and active resolution processes based on the action of so-called specialized pro-resolving mediators (SPMs). These novel lipid mediator molecules derive from the essential ω3-poly-unsaturated fatty acids (PUFAs) DHA and EPA and are synthesized via specific intermediates. The role and benefits of SPMs in chronic inflammatory diseases like obesity, atherosclerosis, and Diabetes mellitus has become a subject of intense research during the last years and since PCOS features several of these pathologies, this review aims at summarizing potential roles of SPMs in this disease and their putative use as novel therapeutics.
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Zaloga, Gary P. "Narrative Review of n-3 Polyunsaturated Fatty Acid Supplementation upon Immune Functions, Resolution Molecules and Lipid Peroxidation." Nutrients 13, no. 2 (February 18, 2021): 662. http://dx.doi.org/10.3390/nu13020662.
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Fish oil supplementation is commonplace in human nutrition and is being used in both enteral and parenteral formulations during the treatment of patients with a large variety of diseases and immune status. The biological effects of fish oil are believed to result from their content of n-3 polyunsaturated fatty acids (PUFA), particularly docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA). These fatty acids are known to have numerous effects upon immune functions and are described as immunomodulatory. However, immunomodulatory is a nondescript term that encompasses immunostimulation and immunosuppression. The primary goal of this review is to better describe the immune effects of n-3 PUFA as they relate to immunostimulatory vs. immunosuppressive effects. One mechanism proposed for the immune effects of n-3 PUFA relates to the production of specialized pro-resolving mediators (SPMs). A second goal of this review is to evaluate the effects of n-3 PUFA supplementation upon production of SPMs. Although n-3 PUFA are stated to possess anti-oxidative properties, these molecules are highly oxidizable due to multiple double bonds and may increase oxidative stress. Thus, the third goal of this review is to evaluate the effects of n-3 PUFA upon lipid oxidation. We conclude, based upon current scientific evidence, that n-3 PUFA suppress inflammatory responses and most cellular immune responses such as chemotaxis, transmigration, antigen presentation, and lymphocyte functions and should be considered immunosuppressive. n-3 PUFA induced production of resolution molecules is inconsistent with many resolution molecules failing to respond to n-3 PUFA supplementation. n-3 PUFA supplementation is associated with increased lipid peroxidation in most studies. Vitamin E co-administration is unreliable for prevention of the lipid peroxidation. These effects should be considered when administering n-3 PUFA to patients that may be immunosuppressed or under high oxidative stress due to illness or other treatments.
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Barker, Grant, Christiaan Leeuwenburgh, Todd Brusko, Lyle Moldawer, Srinivasa T. Reddy, and Faheem W. Guirgis. "Lipid and Lipoprotein Dysregulation in Sepsis: Clinical and Mechanistic Insights into Chronic Critical Illness." Journal of Clinical Medicine 10, no. 8 (April 14, 2021): 1693. http://dx.doi.org/10.3390/jcm10081693.
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In addition to their well-characterized roles in metabolism, lipids and lipoproteins have pleiotropic effects on the innate immune system. These undergo clinically relevant alterations during sepsis and acute inflammatory responses. High-density lipoprotein (HDL) plays an important role in regulating the immune response by clearing bacterial toxins, supporting corticosteroid release, decreasing platelet aggregation, inhibiting endothelial cell apoptosis, reducing the monocyte inflammatory response, and inhibiting expression of endothelial cell adhesion molecules. It undergoes quantitative as well as qualitative changes which can be measured using the HDL inflammatory index (HII). Pro-inflammatory, or dysfunctional HDL (dysHDL) lacks the ability to perform these functions, and we have also found it to independently predict adverse outcomes and organ failure in sepsis. Another important class of lipids known as specialized pro-resolving mediators (SPMs) positively affect the escalation and resolution of inflammation in a temporal fashion. These undergo phenotypic changes in sepsis and differ significantly between survivors and non-survivors. Certain subsets of sepsis survivors go on to have perilous post-hospitalization courses where this inflammation continues in a low grade fashion. This is associated with immunosuppression in a syndrome of persistent inflammation, immunosuppression, and catabolism syndrome (PICS). The continuous release of tissue damage-related patterns and viral reactivation secondary to immunosuppression feed this chronic cycle of inflammation. Animal data indicate that dysregulation of endogenous lipids and SPMs play important roles in this process. Lipids and their associated pathways have been the target of many clinical trials in recent years which have not shown mortality benefit. These results are limited by patient heterogeneity and poor animal models. Considerations of sepsis phenotypes and novel biomarkers in future trials are important factors to be considered in future research. Further characterization of lipid dysregulation and chronic inflammation during sepsis will aid mortality risk stratification, detection of sepsis, and inform individualized pharmacologic therapies.
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Shang, Pei, Ying Zhang, Di Ma, Yulei Hao, Xinyu Wang, Meiying Xin, Yunhai Zhang, Mingqin Zhu, and Jiachun Feng. "Inflammation resolution and specialized pro-resolving lipid mediators in CNS diseases." Expert Opinion on Therapeutic Targets 23, no. 11 (November 2, 2019): 967–86. http://dx.doi.org/10.1080/14728222.2019.1691525.
Full textDissertations / Theses on the topic "Specialized pro-resolution molecules"
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Turner, Lisa A. "Profiling Precursor Lipids for Specialized Pro-Resolution Molecules in Platelet-Rich Plasma Following Fish Oil and Aspirin Intake." VCU Scholars Compass, 2017. http://scholarscompass.vcu.edu/etd/4763.
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Background: Unfavorable outcomes following periodontal surgeries can be attributed to impaired resolution mechanisms likely due to decreased levels of specialized pro-resolution molecules (SPM). The current study investigates if SPM substrate pools in platelet-rich plasma preparations (PRP) can be increased by essential fatty acid (EFA) and / or aspirin supplementation. Methods: Nineteen healthy volunteers were randomly assigned to take i) aspirin; ii) EFA; iii) aspirin and EFA. Four hours after intake, the lipid precursor pools in PRP were quantified using combined Liquid Chromatography tandem mass spectrometry (LC-MS/MS) and the data statistically analyzed using ANCOVA. Results: Of the 77 metabolites screened, only FFA (18:3) showed a significant interaction effect (p=0.019). By itself, neither EFA (p>0.9) nor aspirin (p>0.4) showed any difference (P>0.4). Multiple comparisons could not identify the differences between groups. Conclusions: There is inadequate data to support oral supplementation of EFA and /or aspirin to increase SPM levels in PRP.
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McCormack, Danielle M. "Profiling Precursor Lipids for Specialized Pro-Resolution Molecules in Platelet-Rich Fibrin Following Fish Oil and Aspirin Intake." VCU Scholars Compass, 2017. http://scholarscompass.vcu.edu/etd/4761.
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Background: Current research has demonstrated that aspirin and fish oil (EFA) increase plasma levels of specialized pro-resolution molecules (SPMs). This study investigates their effects on SPM precursor pools in platelet rich fibrin (PRF). Methods: Twenty healthy volunteers were randomly assigned to take aspirin; EFA or aspirin and EFA. Four hours later, SPM precursor levels were quantified using combined Liquid Chromatography tandem mass spectrometry. The differences between the groups: Aspirin (yes or no), EFA (yes or no), were analyzed by ANCOVA, testing for group differences after covarying out the baseline value. Results: There were 4 significant interactions, 1 with an aspirin effect, 2 with an EFA effect, and 64 with no difference between the groups. The significant interaction effect was found for the following lipidome: LPE(20:4), LPI(16:1), LPI(18:1), and LPI(20:3). Aspirin decreased the LPG(16:4) levels, and EFA decreased the LPE(22:5) and PG(16:0/18:0) lipidomes. Conclusions: Some SPM precursor pools in PRF were increased following supplementation.