Journal articles: 'Lipid Mediators of Inflammation (LMI)'

1

Alderton, Gemma. "Lipid mediators of inflammation." Science 371, no. 6526 (January 14, 2021): 248.9–250. http://dx.doi.org/10.1126/science.371.6526.248-i.

Full text

APA, Harvard, Vancouver, ISO, and other styles

2

Robinson, Dwight R. "Lipid Mediators of Inflammation." Rheumatic Disease Clinics of North America 13, no. 2 (August 1987): 385–405. http://dx.doi.org/10.1016/s0889-857x(21)00854-1.

Full text

APA, Harvard, Vancouver, ISO, and other styles

3

Raizman, Michael B. "New Trends in Lipid Mediators Research, vol 5, Lipid Mediators in Eye Inflammation." Archives of Ophthalmology 109, no. 10 (October 1, 1991): 1361. http://dx.doi.org/10.1001/archopht.1991.01080100041026.

Full text

APA, Harvard, Vancouver, ISO, and other styles

4

Wallace, J. L. "Lipid mediators of inflammation in gastric ulcer." American Journal of Physiology-Gastrointestinal and Liver Physiology 258, no. 1 (January 1, 1990): G1—G11. http://dx.doi.org/10.1152/ajpgi.1990.258.1.g1.

Full text

Abstract:

The interest in lipid mediators of inflammation as potential contributors to the pathogenesis of gastric ulcer has increased markedly over the past 20 yr. Although a great deal is known about the actions of mediators such as leukotrienes, thromboxane, and platelet-activating factor in experimental models of ulceration, evidence supporting a role for these mediators in human gastric ulcer is sorely lacking. This review attempts to answer a number of questions regarding the contribution of these mediators to the pathogenesis of gastric ulceration and the possible use of specific inhibitors, antagonists, and dietary manipulation in the treatment of gastric ulcer. Potential directions for future research in this field are suggested as are some of the pitfalls to be avoided in such studies.

APA, Harvard, Vancouver, ISO, and other styles

5

Serhan, Charles N., Nan Chiang, Jesmond Dalli, and Bruce D. Levy. "Lipid Mediators in the Resolution of Inflammation." Cold Spring Harbor Perspectives in Biology 7, no. 2 (October 30, 2014): a016311. http://dx.doi.org/10.1101/cshperspect.a016311.

Full text

APA, Harvard, Vancouver, ISO, and other styles

6

Rocha, Paulo N., Troy J. Plumb, and Thomas M. Coffman. "Eicosanoids: lipid mediators of inflammation in transplantation." Springer Seminars in Immunopathology 25, no. 2 (September 1, 2003): 215–27. http://dx.doi.org/10.1007/s00281-003-0132-4.

Full text

APA, Harvard, Vancouver, ISO, and other styles

7

González-Périz, Ana, and Joan Clària. "Resolution of Adipose Tissue Inflammation." Scientific World JOURNAL 10 (2010): 832–56. http://dx.doi.org/10.1100/tsw.2010.77.

Full text

Abstract:

The presence of the so-called “low-grade” inflammatory state is recognized as a critical event in adipose tissue dysfunction in obesity. This chronic “low-grade” inflammation in white adipose tissue is powerfully augmented through the infiltration of macrophages, which, together with adipocytes, perpetuate a vicious cycle of macrophage recruitment and secretion of free fatty acids and deleterious adipokines that predispose the development of obesity-related comorbidities, such as insulin resistance and nonalcoholic fatty liver disease. In the last decade, many factors have been identified that contribute to mounting uncontrolled inflammation in obese adipose tissue. Among them, bioactive lipid mediators derived from the cyclooxygenase and 5-lipoxygenase pathways, which convert the ω-6-polyunsaturated fatty acid (PUFA) arachidonic acid into potent proinflammatory eicosanoids (i.e., prostaglandins [PGs] and leukotrienes), have emerged. Interestingly, the same lipid mediators that initially trigger the inflammatory response also signal the termination of inflammation by stimulating the biosynthesis of anti-inflammatory and proresolving lipid autacoids. This review discusses the current status, characteristics, and progress in this class of “stop signals”, including the lipoxins, which were the first identified ω-6 PUFA–derived lipid mediators with potent anti-inflammatory properties; the recently described ω-3 PUFA–derived lipid mediators resolvins and protectins; and the cyclopentenone PGs of the D series. Special emphasis is given to the participation of these bioactive lipid autacoids in the resolution of adipose tissue inflammation and in preventing the development of obesity-related complications.

APA, Harvard, Vancouver, ISO, and other styles

8

Bannenberg, Gerhard, Makoto Arita, and Charles N. Serhan. "Endogenous Receptor Agonists: Resolving Inflammation." Scientific World JOURNAL 7 (2007): 1440–62. http://dx.doi.org/10.1100/tsw.2007.188.

Full text

Abstract:

Controlled resolution or the physiologic resolution of a well-orchestrated inflammatory response at the tissue level is essential to return to homeostasis. A comprehensive understanding of the cellular and molecular events that control the termination of acute inflammation is needed in molecular terms given the widely held view that aberrant inflammation underlies many common diseases. This review focuses on recent advances in the understanding of the role of arachidonic acid and ω-3 polyunsaturated fatty acids (PUFA)–derived lipid mediators in regulating the resolution of inflammation. Using a functional lipidomic approach employing LC-MS-MS–based informatics, recent studies, reviewed herein, uncovered new families of local-acting chemical mediators actively biosynthesized during the resolution phase from the essential fatty acids eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). These new families of local chemical mediators are generated endogenously in exudates collected during the resolution phase, and were coined resolvins and protectins because specific members of these novel chemical families control both the duration and magnitude of inflammation in animal models of complex diseases. Recent advances on the biosynthesis, receptors, and actions of these novel anti-inflammatory and proresolving lipid mediators are reviewed with the aim to bring to attention the important role of specific lipid mediators as endogenous agonists in inflammation resolution.

APA, Harvard, Vancouver, ISO, and other styles

9

Ramon, Sesquile, Charles Serhan, and Richard Phipps. "Actions of novel inflammation-resolving lipid mediators on human B cells (112.12)." Journal of Immunology 186, no. 1_Supplement (April 1, 2011): 112.12. http://dx.doi.org/10.4049/jimmunol.186.supp.112.12.

Full text

Abstract:

Abstract The resolution of inflammation is an active and dynamic process. Newly identified lipid mediators are now recognized as key players during the process of inflammation resolution. These lipid-derived molecules constitute four families of endogenous mediators (lipoxins, resolvins, protectins and maresins) derived from essential fatty acids. New findings also demonstrated that these lipid mediators regulate aspects of the immune response, including inhibition of neutrophil infiltration, reduction of T cell cytokine production and stimulation of macrophage phagocytic activity. Their actions on B lymphocytes are not known. Our results indicate that the lipoxin B4 and 17-HDHA, used at 100nM, increase the ability of normal human B cells to produce IgM and IgG when activated with CpG plus anti-IgM. The two lipid mediators also enhance B cell differentiation towards antibody secreting cells. In addition, resolvin D1 and aspirin-triggered resolvin increase antibody production in CpG-stimulated B cells. None of these inflammation resolution lipid mediators affect proliferation and are non-toxic to B cells. Increase of plasma cell differentiation and antibody production coincides with the known involvement of pro-resolving mediators during the late stages of inflammation and pathogen clearance.

APA, Harvard, Vancouver, ISO, and other styles

10

Knuplez, Eva, Eva Maria Sturm, and Gunther Marsche. "Emerging Role of Phospholipase-Derived Cleavage Products in Regulating Eosinophil Activity: Focus on Lysophospholipids, Polyunsaturated Fatty Acids and Eicosanoids." International Journal of Molecular Sciences 22, no. 9 (April 21, 2021): 4356. http://dx.doi.org/10.3390/ijms22094356.

Full text

Abstract:

Eosinophils are important effector cells involved in allergic inflammation. When stimulated, eosinophils release a variety of mediators initiating, propagating, and maintaining local inflammation. Both, the activity and concentration of secreted and cytosolic phospholipases (PLAs) are increased in allergic inflammation, promoting the cleavage of phospholipids and thus the production of reactive lipid mediators. Eosinophils express high levels of secreted phospholipase A2 compared to other leukocytes, indicating their direct involvement in the production of lipid mediators during allergic inflammation. On the other side, eosinophils have also been recognized as crucial mediators with regulatory and homeostatic roles in local immunity and repair. Thus, targeting the complex network of lipid mediators offer a unique opportunity to target the over-activation and ‘pro-inflammatory’ phenotype of eosinophils without compromising the survival and functions of tissue-resident and homeostatic eosinophils. Here we provide a comprehensive overview of the critical role of phospholipase-derived lipid mediators in modulating eosinophil activity in health and disease. We focus on lysophospholipids, polyunsaturated fatty acids, and eicosanoids with exciting new perspectives for future drug development.

APA, Harvard, Vancouver, ISO, and other styles

11

King, Stephen. "Lipid mediators - key or marginal roles in inflammation?" Inpharma Weekly &NA;, no. 872 (January 1993): 8–9. http://dx.doi.org/10.2165/00128413-199308720-00020.

Full text

APA, Harvard, Vancouver, ISO, and other styles

12

Nolan, E., Y. M. O'Meara, and C. Godson. "Lipid mediators of inflammation in obesity-related glomerulopathy." Nephrology Dialysis Transplantation 28, suppl 4 (September 29, 2013): iv22—iv29. http://dx.doi.org/10.1093/ndt/gft392.

Full text

APA, Harvard, Vancouver, ISO, and other styles

13

Spite, Matthew, and Charles N. Serhan. "Novel Lipid Mediators Promote Resolution of Acute Inflammation." Circulation Research 107, no. 10 (November 12, 2010): 1170–84. http://dx.doi.org/10.1161/circresaha.110.223883.

Full text

APA, Harvard, Vancouver, ISO, and other styles

14

Nakamura, Akari, Kento Otani, and Takashi Shichita. "Lipid mediators and sterile inflammation in ischemic stroke." International Immunology 32, no. 11 (April 10, 2020): 719–25. http://dx.doi.org/10.1093/intimm/dxaa027.

Full text

Abstract:

Abstract Stroke is one of the major causes of lethality and disability, yet few effective therapies have been established for ischemic stroke. Inflammation in the ischemic brain is induced by the infiltration and subsequent activation of immune cells. Loss of cerebral blood flow and ischemic brain-cell death trigger the activation of infiltrating immune cells and drastic changes in the lipid content of the ischemic brain. In particular, polyunsaturated fatty acids and their metabolites regulate cerebral post-ischemic inflammation and ischemic stroke pathologies. In this review, we discuss the relationships between the lipid mediators and cerebral post-ischemic inflammation and their relevance to possible future therapeutic strategies targeting lipid mediators for ischemic stroke.

APA, Harvard, Vancouver, ISO, and other styles

15

Kendall, Alexandra C., and Anna Nicolaou. "Bioactive lipid mediators in skin inflammation and immunity." Progress in Lipid Research 52, no. 1 (January 2013): 141–64. http://dx.doi.org/10.1016/j.plipres.2012.10.003.

Full text

APA, Harvard, Vancouver, ISO, and other styles

16

Goh, Jason, Catherine Godson, Hugh R. Brady, and Padraic MacMathuna. "Lipoxins: Pro-resolution lipid mediators in intestinal inflammation." Gastroenterology 124, no. 4 (April 2003): 1043–54. http://dx.doi.org/10.1053/gast.2003.50154.

Full text

APA, Harvard, Vancouver, ISO, and other styles

17

Fullerton, James N., Alastair J. O’Brien, and Derek W. Gilroy. "Lipid mediators in immune dysfunction after severe inflammation." Trends in Immunology 35, no. 1 (January 2014): 12–21. http://dx.doi.org/10.1016/j.it.2013.10.008.

Full text

APA, Harvard, Vancouver, ISO, and other styles

18

Phipps, Richard, Thomas Thatcher, Hsi-Min Hsiao, Charles Serhan, and Patricia Sime. "Pro-resolving lipid mediators attenuate lung inflammation (P5080)." Journal of Immunology 190, no. 1_Supplement (May 1, 2013): 180.23. http://dx.doi.org/10.4049/jimmunol.190.supp.180.23.

Full text

Abstract:

Abstract Introduction: Cigarette smoking is the major world-wide cause of COPD and other inflammatory diseases. COPD persists after smoking cessation, suggesting that this may be a failure to resolve inflammation. Resolution of inflammation is an active process regulated by small lipid mediators derived mainly from omega-3 polyunsaturated fatty acids, including the resolvins, and others. We hypothesized that resolvin D1 (RvD1) would have anti-inflammatory and pro-resolving effects in cigarette smoke-induced lung inflammation. Methods: Primary human lung cells (e.g. fibroblasts, etc) were treated with cigarette smoke extract and RvD1 in vitro, and production of pro-inflammatory mediators was determined. Mice were exposed to dilute mainstream cigarette smoke and treated with RvD1 either concurrently with smoke or after smoking cessation. The effect on lung inflammation was assessed. Results: RvD1 suppressed production of pro-inflammatory mediators by human cells. Treatment of mice with RvD1 concurrently with cigarette smoke exposure significantly reduced neutrophilic lung inflammation and production of pro-inflammatory cytokines. RvD1 promoted differentiation of alternatively activated (M2) macrophages. RvD1 also accelerated the resolution of lung inflammation when given after the final smoke exposure. Conclusions: RvD1 has potent pro-resolving effects in cells and mice exposed to cigarette smoke. Resolvins may be a novel therapeutic approach to resolve lung injury and disease.

APA, Harvard, Vancouver, ISO, and other styles

19

Miki, Yoshimi, Kei Yamamoto, Yoshitaka Taketomi, Hiroyasu Sato, Kanako Shimo, Tetsuyuki Kobayashi, Yukio Ishikawa, et al. "Lymphoid tissue phospholipase A2 group IID resolves contact hypersensitivity by driving antiinflammatory lipid mediators." Journal of Experimental Medicine 210, no. 6 (May 20, 2013): 1217–34. http://dx.doi.org/10.1084/jem.20121887.

Full text

Abstract:

Resolution of inflammation is an active process that is mediated in part by antiinflammatory lipid mediators. Although phospholipase A2 (PLA2) enzymes have been implicated in the promotion of inflammation through mobilizing lipid mediators, the molecular entity of PLA2 subtypes acting upstream of antiinflammatory lipid mediators remains unknown. Herein, we show that secreted PLA2 group IID (PLA2G2D) is preferentially expressed in CD11c+ dendritic cells (DCs) and macrophages and displays a pro-resolving function. In hapten-induced contact dermatitis, resolution, not propagation, of inflammation was compromised in skin and LNs of PLA2G2D-deficient mice (Pla2g2d−/−), in which the immune balance was shifted toward a proinflammatory state over an antiinflammatory state. Bone marrow-derived DCs from Pla2g2d−/− mice were hyperactivated and elicited skin inflammation after intravenous transfer into mice. Lipidomics analysis revealed that PLA2G2D in the LNs contributed to mobilization of a pool of polyunsaturated fatty acids that could serve as precursors for antiinflammatory/pro-resolving lipid mediators such as resolvin D1 and 15-deoxy-Δ12,14-prostaglandin J2, which reduced Th1 cytokine production and surface MHC class II expression in LN cells or DCs. Altogether, our results highlight PLA2G2D as a “resolving sPLA2” that ameliorates inflammation through mobilizing pro-resolving lipid mediators and points to a potential use of this enzyme for treatment of inflammatory disorders.

APA, Harvard, Vancouver, ISO, and other styles

20

Lu, Yan, Song Hong, Katherine Gotlinger, and Charles Serhan. "Lipid Mediator Informatics and Proteomics in Inflammation-Resolution." Scientific World JOURNAL 6 (2006): 589–614. http://dx.doi.org/10.1100/tsw.2006.118.

Full text

Abstract:

Lipid mediator informatics is an emerging area denoted to the identification of bioactive lipid mediators (LMs) and their biosynthetic profiles and pathways. LM informatics and proteomics applied to inflammation, systems tissues research provides a powerful means of uncovering key biomarkers for novel processes in health and disease. By incorporating them with system biology analysis, we review here our initial steps toward elucidating relationships among a range of bimolecular classes and provide an appreciation of their roles and activities in the pathophysiology of disease. LM informatics employing liquid chromatography-ultraviolet-tandem mass spectrometry (LC-UV-MS/MS), gas chromatography-mass spectrometry (GC-MS), computer-based automated systems equipped with databases and novel searching algorithms, and enzyme-linked immunosorbent assay (ELISA) to evaluate and profile temporal and spatial production of mediators combined with proteomics at defined points during experimental inflammation and its resolution enable us to identify novel mediators in resolution. The automated system including databases and searching algorithms is crucial for prompt and accurate analysis of these lipid mediators biosynthesized from precursor polyunsaturated fatty acids such as eicosanoids, resolvins, and neuroprotectins, which play key roles in human physiology and many prevalent diseases, especially those related to inflammation. This review presents detailed protocols used in our lab for LM informatics and proteomics using LC-UV-MS/MS, GC-MS, ELISA, novel databases and searching algorithms, and 2-dimensional gel electrophoresis and LC-nanospray-MS/MS peptide mapping.

APA, Harvard, Vancouver, ISO, and other styles

21

Lubrano, Valter, Rudina Ndreu, and Silvana Balzan. "Classes of Lipid Mediators and Their Effects on Vascular Inflammation in Atherosclerosis." International Journal of Molecular Sciences 24, no. 2 (January 13, 2023): 1637. http://dx.doi.org/10.3390/ijms24021637.

Full text

Abstract:

It is commonly believed that the inactivation of inflammation is mainly due to the decay or cessation of inducers. In reality, in connection with the development of atherosclerosis, spontaneous decay of inducers is not observed. It is now known that lipid mediators originating from polyunsaturated fatty acids (PUFAs), which are important constituents of all cell membranes, can act in the inflamed tissue and bring it to resolution. In fact, PUFAs, such as arachidonic acid (AA), eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA), are precursors to both pro-inflammatory and anti-inflammatory compounds. In this review, we describe the lipid mediators of vascular inflammation and resolution, and their biochemical activity. In addition, we highlight data from the literature that often show a worsening of atherosclerotic disease in subjects deficient in lipid mediators of inflammation resolution, and we also report on the anti-proteasic and anti-thrombotic properties of these same lipid mediators. It should be noted that despite promising data observed in both animal and in vitro studies, contradictory clinical results have been observed for omega-3 PUFAs. Many further studies will be required in order to clarify the observed conflicts, although lifestyle habits such as smoking or other biochemical factors may often influence the normal synthesis of lipid mediators of inflammation resolution.

APA, Harvard, Vancouver, ISO, and other styles

22

Philippe, Réginald, and Valerie Urbach. "Specialized Pro-Resolving Lipid Mediators in Cystic Fibrosis." International Journal of Molecular Sciences 19, no. 10 (September 21, 2018): 2865. http://dx.doi.org/10.3390/ijms19102865.

Full text

Abstract:

In cystic fibrosis (CF), impaired airway surface hydration (ASL) and mucociliary clearance that promote chronic bacterial colonization, persistent inflammation, and progressive structural damage to the airway wall architecture are typically explained by ion transport abnormalities related to the mutation of the gene coding for the Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) channel. However, the progressive and unrelenting inflammation of the CF airway begins early in life, becomes persistent, and is excessive relative to the bacterial burden. Intrinsic abnormalities of the inflammatory response in cystic fibrosis have been suggested but the mechanisms involved remain poorly understood. This review aims to give an overview of the recent advances in the understanding of the defective resolution of inflammation in CF including the abnormal production of specialized pro-resolving lipid mediators (lipoxin and resolvin) and their impact on the pathogenesis of the CF airway disease.

APA, Harvard, Vancouver, ISO, and other styles

23

van Dijk, A. P. M., Z. J. Keuskamp, J. H. P. Wilson, and F. J. Zijlstra. "Sequential release of cytokines, lipid mediators and nitric oxide in experimental colitis." Mediators of Inflammation 4, no. 3 (1995): 186–90. http://dx.doi.org/10.1155/s0962935195000305.

Full text

Abstract:

The object of this study was to establish whether different pro- and anti-inflammatory mediators were formed in colonic tissue from experimental colitis depending on the course of the disease. Concentrations of mediators of inflammation were examined in colonic tissue in dextran induced colitis in mice. Initial inflammation was produced by 5 days treatment of 10% dextran sodium sulfate (DSS) in drinking water, followed by a further 9 day period of 2% DSS in an attempt to produce a milder chronic inflammation. The degree of inflammation was scored by a standardized macroscopic and histological examination. Initially, a 60% maximum inflammation score was observed at day 4. At this time inflammation was associated with the release of interleukin-lβ (IL-1β) and tumour necrosis factor-α (TNFα), whereas both prostaglandins 6kPGF1αand PGE2and nitric oxide (NO) markedly decreased. Then a 25% inflammation score was reached which coincided with an increased production of platelet-activating factor (PAF). No significant changes were observed in leukotriene B4and C4formation. In conclusion, pro-inflammatory cytokines IL-1β and TNFα are considered to be primary mediators, whereas PAF, eicosanoids and NO may reflect secondary mediators in experimental colitis.

APA, Harvard, Vancouver, ISO, and other styles

24

Ramon, Sesquile, Charles Serhan, and Richard Phipps. "Actions of novel inflammation-resolving lipid mediators on human B cells (84.9)." Journal of Immunology 184, no. 1_Supplement (April 1, 2010): 84.9. http://dx.doi.org/10.4049/jimmunol.184.supp.84.9.

Full text

Abstract:

Abstract The resolution of inflammation is an active and dynamic process. Newly identified lipid mediators have been recognized as key players during the process of inflammation resolution. These lipid-derived molecules constitute three classes of compounds (lipoxins, resolvins and protectins), all derived from essential fatty acids. New data demonstrates that these lipid mediators regulate aspects of the immune response, including inhibition of neutrophil infiltration, reduction of T cell cytokine production and stimulation of macrophage phagocytic activity. However, their effects on B lymphocytes are unknown. We show for the first time that the novel lipid mediator lipoxin B4 and 17-HDHA increase the ability of normal human B cells to produce IgM and IgG when activated with CpG plus anti-IgM. The two lipid derived molecules along with lipoxin A4 also enhance B cell differentiation, measured by an increased frequency of CD38+ cells. In addition, resolvin D1 and AT-resolvin also increase antibody production in CpG-stimulated B cells. None of the inflammation resolution lipid mediators affect proliferation and are non-toxic to the cells. Increase of plasma cell differentiation and antibody production coincides with the known involvement of pro-resolving mediators during the late stages of inflammation and pathogen clearance.

APA, Harvard, Vancouver, ISO, and other styles

25

Serhan, Charles N. "Novel Lipid Mediators and Resolution Mechanisms in Acute Inflammation." American Journal of Pathology 177, no. 4 (October 2010): 1576–91. http://dx.doi.org/10.2353/ajpath.2010.100322.

Full text

APA, Harvard, Vancouver, ISO, and other styles

26

Reina-Couto, Marta, Luís Vale, Jorge Carvalho, Paulo Bettencourt, António Albino-Teixeira, and Teresa Sousa. "Resolving Inflammation in Heart Failure: Novel Protective Lipid Mediators." Current Drug Targets 17, no. 10 (June 24, 2016): 1206–23. http://dx.doi.org/10.2174/1389450117666160101121135.

Full text

APA, Harvard, Vancouver, ISO, and other styles

27

Sommakia, S., and OJ Baker. "Regulation of inflammation by lipid mediators in oral diseases." Oral Diseases 23, no. 5 (August 4, 2016): 576–97. http://dx.doi.org/10.1111/odi.12544.

Full text

APA, Harvard, Vancouver, ISO, and other styles

28

Haworth, O., and B. D. Levy. "Endogenous lipid mediators in the resolution of airway inflammation." European Respiratory Journal 30, no. 5 (November 1, 2007): 980–92. http://dx.doi.org/10.1183/09031936.00005807.

Full text

APA, Harvard, Vancouver, ISO, and other styles

29

Kanter, Jennifer L., Sirisha Narayana, Peggy P. Ho, Ingrid Catz, Kenneth G. Warren, Raymond A. Sobel, Lawrence Steinman, and William H. Robinson. "Lipid microarrays identify key mediators of autoimmune brain inflammation." Nature Medicine 12, no. 1 (December 11, 2005): 138–43. http://dx.doi.org/10.1038/nm1344.

Full text

APA, Harvard, Vancouver, ISO, and other styles

30

Valacchi, Giuseppe, Chiara De Luca, and Philip W. Wertz. "Lipid Mediators in Skin Inflammation: Updates and Current Views." Mediators of Inflammation 2010 (2010): 1–2. http://dx.doi.org/10.1155/2010/398926.

Full text

APA, Harvard, Vancouver, ISO, and other styles

31

Serhan, Charles N., and Nan Chiang. "Resolution phase lipid mediators of inflammation: agonists of resolution." Current Opinion in Pharmacology 13, no. 4 (August 2013): 632–40. http://dx.doi.org/10.1016/j.coph.2013.05.012.

Full text

APA, Harvard, Vancouver, ISO, and other styles

32

Brouwers, Hilde, Joost von Hegedus, René Toes, Margreet Kloppenburg, and Andreea Ioan-Facsinay. "Lipid mediators of inflammation in rheumatoid arthritis and osteoarthritis." Best Practice & Research Clinical Rheumatology 29, no. 6 (December 2015): 741–55. http://dx.doi.org/10.1016/j.berh.2016.02.003.

Full text

APA, Harvard, Vancouver, ISO, and other styles

33

Sumida, Hayakazu, Yoshihiro Kita, Takao Shimizu, and Shinichi Sato. "Novel roles of lipid mediators in psoriatic skin inflammation." Journal of Immunology 202, no. 1_Supplement (May 1, 2019): 182.42. http://dx.doi.org/10.4049/jimmunol.202.supp.182.42.

Full text

Abstract:

Abstract Psoriasis is a common chronic inflammatory cutaneous disease thought to arise as a result of infiltration of inflammatory cells and activation of keratinocytes. Psoriasis has been considered as a classical Th1 disease; however, Th17 cells are attracting much interest. Previous knowledge on the pathology of psoriasis has been obtained mostly through the study of human data and samples. In addition, recently developed animal models for psoriatic skin inflammation recapitulates the hallmarks of human psoriasis and provide us new insights on psoriasis. Lipid mediators and their receptors regulate a variety of physiological processes and involved in multiple pathologies including immune-related diseases. Here, we explored novel lipid mediators involved in psoriatic skin inflammation using clinical samples and imiquimod-induced psoriasis model. In particular, mass spectrometry analysis for multiplex quantitation of eicosanoids using imiquimod-treated murine skin samples revealed unique kinetics of various lipid mediators in the time-series from early induction phase to chronic resolution phase. These data motivated us to focus on some lipid mediators such as leukotriene B4 (LTB4) and prostaglandin E2 (PGE2). As an example, BLT1 (known as LTB4 receptor) and CXCR2 have been revealed to coordinately promote neutrophil infiltration into the skin during the early phase of imiquimod-induced inflammation. Further analysis on PGE2 is in progress and some data indicates the novel functions of PGE2 and mPGES-1, an upstream enzyme for PGE2 production, in the pathogenesis in psoriasis. These insights may aid in the rational design of novel treatments for broad spectrum of inflammatory and immune disorders beyond psoriasis.

APA, Harvard, Vancouver, ISO, and other styles

34

Khan, Shahida A., Ashraf Ali, Sarah A. Khan, Solafa A. Zahran, Ghazi Damanhouri, Esam Azhar, and Ishtiaq Qadri. "Unraveling the Complex Relationship Triad between Lipids, Obesity, and Inflammation." Mediators of Inflammation 2014 (2014): 1–16. http://dx.doi.org/10.1155/2014/502749.

Full text

Abstract:

Obesity today stands at the intersection between inflammation and metabolic disorders causing an aberration of immune activity, and resulting in increased risk for diabetes, atherosclerosis, fatty liver, and pulmonary inflammation to name a few. Increases in mortality and morbidity in obesity related inflammation have initiated studies to explore different lipid mediated molecular pathways of attempting resolution that uncover newer therapeutic opportunities of anti-inflammatory components. Majorly the thromboxanes, prostaglandins, leukotrienes, lipoxins, and so forth form the group of lipid mediators influencing inflammation. Of special mention are the omega-6 and omega-3 fatty acids that regulate inflammatory mediators of interest in hepatocytes and adipocytes via the cyclooxygenase and lipoxygenase pathways. They also exhibit profound effects on eicosanoid production. The inflammatory cyclooxygenase pathway arising from arachidonic acid is a critical step in the progression of inflammatory responses. New oxygenated products of omega-3 metabolism, namely, resolvins and protectins, behave as endogenous mediators exhibiting powerful anti-inflammatory and immune-regulatory actions via the peroxisome proliferator-activated receptors (PPARs) and G protein coupled receptors (GPCRs). In this review we attempt to discuss the complex pathways and links between obesity and inflammation particularly in relation to different lipid mediators.

APA, Harvard, Vancouver, ISO, and other styles

35

Recchiuti, Antonio, Elisa Isopi, Mario Romano, and Domenico Mattoscio. "Roles of Specialized Pro-Resolving Lipid Mediators in Autophagy and Inflammation." International Journal of Molecular Sciences 21, no. 18 (September 10, 2020): 6637. http://dx.doi.org/10.3390/ijms21186637.

Full text

Abstract:

Autophagy is a catabolic pathway that accounts for degradation and recycling of cellular components to extend cell survival under stress conditions. In addition to this prominent role, recent evidence indicates that autophagy is crucially involved in the regulation of the inflammatory response, a tightly controlled process aimed at clearing the inflammatory stimulus and restoring tissue homeostasis. To be efficient and beneficial to the host, inflammation should be controlled by a resolution program, since uncontrolled inflammation is the underlying cause of many pathologies. Resolution of inflammation is an active process mediated by a variety of mediators, including the so-called specialized pro-resolving lipid mediators (SPMs), a family of endogenous lipid autacoids known to regulate leukocyte infiltration and activities, and counterbalance cytokine production. Recently, regulation of autophagic mechanisms by these mediators has emerged, uncovering unappreciated connections between inflammation resolution and autophagy. Here, we summarize mechanisms of autophagy and resolution, focusing on the contribution of autophagy in sustaining paradigmatic examples of chronic inflammatory disorders. Then, we discuss the evidence that SPMs can restore dysregulated autophagy, hypothesizing that resolution of inflammation could represent an innovative approach to modulate autophagy and its impact on the inflammatory response.

APA, Harvard, Vancouver, ISO, and other styles

36

Valente, Mariarosaria, Marta Dentoni, Fabrizio Bellizzi, Fedra Kuris, and Gian Luigi Gigli. "Specialized Pro-Resolving Mediators in Neuroinflammation: Overview of Studies and Perspectives of Clinical Applications." Molecules 27, no. 15 (July 28, 2022): 4836. http://dx.doi.org/10.3390/molecules27154836.

Full text

Abstract:

Specialized pro-resolving mediators (SPMs) are lipid mediators derived from poly-unsaturated fatty acids (PUFAs) which have been demonstrated to have an important role in the inflammation environment, preventing an overreaction of the organism and promoting the resolution of inflammation. Our purpose was to point out the current evidence for specialized pro-resolving mediators, focusing on their role in neuroinflammation and in major neurological diseases.

APA, Harvard, Vancouver, ISO, and other styles

37

Serhan, Charles N., Nan Chiang, and Thomas E. Van Dyke. "Resolving inflammation: dual anti-inflammatory and pro-resolution lipid mediators." Nature Reviews Immunology 8, no. 5 (May 2008): 349–61. http://dx.doi.org/10.1038/nri2294.

Full text

APA, Harvard, Vancouver, ISO, and other styles

38

Clària, Joan. "Resolution of Acute Inflammation and the Role of Lipid Mediators." Scientific World JOURNAL 10 (2010): 1553–55. http://dx.doi.org/10.1100/tsw.2010.157.

Full text

APA, Harvard, Vancouver, ISO, and other styles

39

Iyer, Abishek, and Lindsay Brown. "Lipid mediators and inflammation in glucose intolerance and insulin resistance." Drug Discovery Today: Disease Mechanisms 7, no. 3-4 (December 2010): e191-e197. http://dx.doi.org/10.1016/j.ddmec.2010.12.001.

Full text

APA, Harvard, Vancouver, ISO, and other styles

40

SCHWAB, J., and C. SERHAN. "Lipoxins and new lipid mediators in the resolution of inflammation." Current Opinion in Pharmacology 6, no. 4 (August 2006): 414–20. http://dx.doi.org/10.1016/j.coph.2006.02.006.

Full text

APA, Harvard, Vancouver, ISO, and other styles

41

Devitt, Andrew, Helen R. Griffiths, and Ivana Milic. "Communicating with the dead: lipids, lipid mediators and extracellular vesicles." Biochemical Society Transactions 46, no. 3 (May 9, 2018): 631–39. http://dx.doi.org/10.1042/bst20160477.

Full text

Abstract:

Apoptosis is a key event in the control of inflammation. However, for this to be successful, dying cells must efficiently and effectively communicate their presence to phagocytes to ensure timely removal of dying cells. Here, we consider apoptotic cell-derived extracellular vesicles and the role of contained lipids and lipid mediators in ensuring effective control of inflammation. We discuss key outstanding issues in the study of cell death and cell communication, and introduce the concept of the ‘active extracellular vesicle’ as a metabolically active and potentially changing intercellular communicator.

APA, Harvard, Vancouver, ISO, and other styles

42

Kytikova, Oxana, Tatyana Novgorodtseva, Yulia Denisenko, Marina Antonyuk, and Tatyana Gvozdenko. "Pro-Resolving Lipid Mediators in the Pathophysiology of Asthma." Medicina 55, no. 6 (June 18, 2019): 284. http://dx.doi.org/10.3390/medicina55060284.

Full text

Abstract:

Asthma is one of the most important medical and social problems of our time due to the prevalence and the complexity of its treatment. Chronic inflammation that is characteristic of asthma is accompanied by bronchial obstruction, which involves various lipid mediators produced from n-6 and n-3 polyunsaturated fatty acids (PUFAs). The review is devoted to modern ideas about the PUFA metabolites—eicosanoids (leukotrienes, prostaglandins, thromboxanes) and specialized pro-resolving lipid mediators (SPMs) maresins, lipoxins, resolvins, protectins. The latest advances in clinical lipidomics for identifying and disclosing the mechanism of synthesis and the biological action of SPMs have been given. The current views on the peculiarities of the inflammatory reaction in asthma and the role of highly specialized metabolites of arachidonic, eicosapentaenoic and docosahexaenoic acids in this process have been described. The possibility of using SPMs as therapeutic agents aimed at controlling the resolution of inflammation in asthma is discussed.

APA, Harvard, Vancouver, ISO, and other styles

43

Kotlyarov, Stanislav, and Anna Kotlyarova. "Anti-Inflammatory Function of Fatty Acids and Involvement of Their Metabolites in the Resolution of Inflammation in Chronic Obstructive Pulmonary Disease." International Journal of Molecular Sciences 22, no. 23 (November 26, 2021): 12803. http://dx.doi.org/10.3390/ijms222312803.

Full text

Abstract:

Lipid metabolism plays an important role in many lung functions. Disorders of lipid metabolism are part of the pathogenesis of chronic obstructive pulmonary disease (COPD). Lipids are involved in numerous cross-linkages with inflammation. Recent studies strongly support the involvement of fatty acids as participants in inflammation. They are involved in the initiation and resolution of inflammation, including acting as a substrate for the formation of lipid mediators of inflammation resolution. Specialized pro-inflammatory mediators (SPMs) belonging to the classes of lipoxins, resolvins, maresins, and protectins, which are formed enzymatically from unsaturated fatty acids, are now described. Disorders of their production and function are part of the pathogenesis of COPD. SPMs are currently the subject of active research in order to find new drugs. Short-chain fatty acids are another important participant in metabolic and immune processes, and their role in the pathogenesis of COPD is of great clinical interest.

APA, Harvard, Vancouver, ISO, and other styles

44

Bozza, Patricia T., Wengui Yu, John F. Penrose, Ellen S. Morgan, Ann M. Dvorak, and Peter F. Weller. "Eosinophil Lipid Bodies: Specific, Inducible Intracellular Sites for Enhanced Eicosanoid Formation." Journal of Experimental Medicine 186, no. 6 (September 15, 1997): 909–20. http://dx.doi.org/10.1084/jem.186.6.909.

Full text

Abstract:

The specific intracellular sites at which enzymes act to generate arachidonate-derived eicosanoid mediators of inflammation are uncertain. We evaluated the formation and function of cytoplasmic lipid bodies. Lipid body formation in eosinophils was a rapidly (<1 h) inducible response which was platelet-activating factor (PAF) receptor–mediated, involved signaling through protein kinase C, and required new protein synthesis. In intact and enucleated eosinophils, the PAF-induced increases in lipid body numbers correlated with enhanced production of both lipoxygenase- and cyclooxygenase-derived eicosanoids. All principal eosinophil eicosanoid-forming enzymes, 5-lipoxygenase, leukotriene C4 synthase, and cyclooxygenase, were immunolocalized to native as well as newly induced lipid bodies in intact and enucleated eosinophils. Thus, lipid bodies are structurally distinct, inducible, nonnuclear sites for enhanced synthesis of paracrine eicosanoid mediators of inflammation.

APA, Harvard, Vancouver, ISO, and other styles

45

Merularini, Saravanan, Madhuram Krishnamurthy, Ashok Leburu, Praveen Nehrudas, Selvendran K. Elangovan, and Naveen Kumar Venugopal. "Specialized pro-resolving lipid mediators: A future for conventional endodontics-A review." IP Indian Journal of Conservative and Endodontics 7, no. 3 (October 15, 2022): 105–8. http://dx.doi.org/10.18231/j.ijce.2022.023.

Full text

Abstract:

Human dental pulp is a highly dynamic tissue that plays major roles in the defense against pathogens and during tissue injury. However, the efficiency of these mechanisms during dental pulp inflammation (pulpitis) varies due to anatomical and physiological restrictions. Uncontrolled progressive unresolved inflammation can lead to pulp tissue necrosis and subsequent apical periodontitis or it can develop into chronic inflammation and become a silent killer causing bone destruction. Considering the cause & effect model, the decision to perform pulp extirpation and endodontic treatment is justifiable only by the lack of therapeutic tools that limit the immune/inflammatory process. The resolution of acute inflammation is necessary to avoid the development of chronic inflammation and to promote repair or regeneration. This active process is orchestrated by Specialized Pro-resolving lipid Mediators (SPMs), which include several families of distinct local mediators (lipoxins, resolvins, protectins and Maresins). These immunoresolvents are distinct from immunosuppressive molecules as they not only dampen inflammation but also promote host defense. Experimental application of SPMs has shown promising result in wide range of inflammatory diseases. This article illustrates about the potential use of SPMs in dentistry

APA, Harvard, Vancouver, ISO, and other styles

46

Díaz del Campo, Lucía Serrano, Raquel Rodrigues-Díez, Mercedes Salaices, Ana M. Briones, and Ana B. García-Redondo. "Specialized Pro-Resolving Lipid Mediators: New Therapeutic Approaches for Vascular Remodeling." International Journal of Molecular Sciences 23, no. 7 (March 25, 2022): 3592. http://dx.doi.org/10.3390/ijms23073592.

Full text

Abstract:

Vascular remodeling is a typical feature of vascular diseases, such as atherosclerosis, aneurysms or restenosis. Excessive inflammation is a key mechanism underlying vascular remodeling via the modulation of vascular fibrosis, phenotype and function. Recent evidence suggests that not only augmented inflammation but unresolved inflammation might also contribute to different aspects of vascular diseases. Resolution of inflammation is mediated by a family of specialized pro-resolving mediators (SPMs) that limit immune cell infiltration and initiate tissue repair mechanisms. SPMs (lipoxins, resolvins, protectins, maresins) are generated from essential polyunsaturated fatty acids. Synthases and receptors for SPMs were initially described in immune cells, but they are also present in endothelial cells (ECs) and vascular smooth muscle cells (VSMCs), where they regulate processes important for vascular physiology, such as EC activation and VSMC phenotype. Evidence from genetic models targeting SPM pathways and pharmacological supplementation with SPMs have demonstrated that these mediators may play a protective role against the development of vascular remodeling in atherosclerosis, aneurysms and restenosis. This review focuses on the latest advances in understanding the role of SPMs in vascular cells and their therapeutic effects in the vascular remodeling associated with different cardiovascular diseases.

APA, Harvard, Vancouver, ISO, and other styles

47

Tang, Shi, Ming Wan, Wei Huang, R. C. Stanton, and Yong Xu. "Maresins: Specialized Proresolving Lipid Mediators and Their Potential Role in Inflammatory-Related Diseases." Mediators of Inflammation 2018 (2018): 1–8. http://dx.doi.org/10.1155/2018/2380319.

Full text

Abstract:

Acute inflammatory responses are host-protective and normally self-limited; these responses can maintain cell homeostasis and promote defense against various infections and damage factors. However, when improperly managed or inappropriately activated, acute inflammation can lead to persistent and uncontrolled chronic inflammation, which is associated with many other chronic diseases including cardiovascular disease and metabolic disease. Recently, studies have shown that resolution of acute inflammation is a biosynthetically active process. Specialized proresolving lipid mediators (SPMs) known as resolvins and protectins are autacoids that resolve inflammation. A new family of anti-inflammatory and proresolving lipid mediators have recently been reported, known as maresins, which are biosynthesized from docosahexaenoic acid (DHA) by macrophages, have a conjugated double-bond system, and display strong anti-inflammatory and proresolving activity. Here, we review the biological actions, pathways, and mechanisms of maresins, which may play pivotal roles in the resolution of inflammation.

APA, Harvard, Vancouver, ISO, and other styles

48

Flitter, Becca A., Kelli L. Hvorecny, Emiko Ono, Taylor Eddens, Jun Yang, Daniel H. Kwak, Christopher D. Bahl, et al. "Pseudomonas aeruginosa sabotages the generation of host proresolving lipid mediators." Proceedings of the National Academy of Sciences 114, no. 1 (December 15, 2016): 136–41. http://dx.doi.org/10.1073/pnas.1610242114.

Full text

Abstract:

Recurrent Pseudomonas aeruginosa infections coupled with robust, damaging neutrophilic inflammation characterize the chronic lung disease cystic fibrosis (CF). The proresolving lipid mediator, 15-epi lipoxin A4 (15-epi LXA4), plays a critical role in limiting neutrophil activation and tissue inflammation, thus promoting the return to tissue homeostasis. Here, we show that a secreted P. aeruginosa epoxide hydrolase, cystic fibrosis transmembrane conductance regulator inhibitory factor (Cif), can disrupt 15-epi LXA4 transcellular biosynthesis and function. In the airway, 15-epi LXA4 production is stimulated by the epithelial-derived eicosanoid 14,15-epoxyeicosatrienoic acid (14,15-EET). Cif sabotages the production of 15-epi LXA4 by rapidly hydrolyzing 14,15-EET into its cognate diol, eliminating a proresolving signal that potently suppresses IL-8–driven neutrophil transepithelial migration in vitro. Retrospective analyses of samples from patients with CF supported the translational relevance of these preclinical findings. Elevated levels of Cif in bronchoalveolar lavage fluid were correlated with lower levels of 15-epi LXA4, increased IL-8 concentrations, and impaired lung function. Together, these findings provide structural, biochemical, and immunological evidence that the bacterial epoxide hydrolase Cif disrupts resolution pathways during bacterial lung infections. The data also suggest that Cif contributes to sustained pulmonary inflammation and associated loss of lung function in patients with CF.

APA, Harvard, Vancouver, ISO, and other styles

49

Barnig, Cindy, Gaetan Lutzweiler, Margherita Giannini, Anne Lejay, Anne-Laure Charles, Alain Meyer, and Bernard Geny. "Resolution of Inflammation after Skeletal Muscle Ischemia–Reperfusion Injury: A Focus on the Lipid Mediators Lipoxins, Resolvins, Protectins and Maresins." Antioxidants 11, no. 6 (June 20, 2022): 1213. http://dx.doi.org/10.3390/antiox11061213.

Full text

Abstract:

Skeletal muscle ischemia reperfusion is very frequent in humans and results not only in muscle destruction but also in multi-organ failure and death via systemic effects related to inflammation and oxidative stress. In addition to overabundance of pro-inflammatory stimuli, excessive and uncontrolled inflammation can also result from defects in resolution signaling. Importantly, the resolution of inflammation is an active process also based on specific lipid mediators including lipoxins, resolvins and maresins that orchestrate the potential return to tissue homeostasis. Thus, lipid mediators have received growing attention since they dampen deleterious effects related to ischemia–reperfusion. For instance, the treatment of skeletal muscles with resolvins prior to ischemia decreases polymorphonuclear leukocyte (PMN) infiltration. Additionally, remote alterations in lungs or kidneys are reduced when enhancing lipid mediators’ functions. Accordingly, lipoxins prevented oxidative-stress-mediated tissue injuries, macrophage polarization was modified and in mice lacking DRV2 receptors, ischemia/reperfusion resulted in excessive leukocyte accumulation. In this review, we first aimed to describe the inflammatory response during ischemia and reperfusion in skeletal muscle and then discuss recent discoveries in resolution pathways. We focused on the role of specialized pro-resolving mediators (SPMs) derived from polyunsaturated fatty acids (PUFAs) and their potential therapeutic applications.

APA, Harvard, Vancouver, ISO, and other styles

50

Liu, Tianye, Alec Xiang, Travis Peng, Amanda C. Doran, Kevin J. Tracey, Betsy J. Barnes, Ira Tabas, Myoungsun Son, and Betty Diamond. "HMGB1–C1q complexes regulate macrophage function by switching between leukotriene and specialized proresolving mediator biosynthesis." Proceedings of the National Academy of Sciences 116, no. 46 (September 30, 2019): 23254–63. http://dx.doi.org/10.1073/pnas.1907490116.

Full text

Abstract:

Macrophage polarization is critical to inflammation and resolution of inflammation. We previously showed that high-mobility group box 1 (HMGB1) can engage receptor for advanced glycation end product (RAGE) to direct monocytes to a proinflammatory phenotype characterized by production of type 1 IFN and proinflammatory cytokines. In contrast, HMGB1 plus C1q form a tetramolecular complex cross-linking RAGE and LAIR-1 and directing monocytes to an antiinflammatory phenotype. Lipid mediators, as well as cytokines, help establish a milieu favoring either inflammation or resolution of inflammation. This study focuses on the induction of lipid mediators by HMGB1 and HMGB1 plus C1q and their regulation of IRF5, a transcription factor critical for the induction and maintenance of proinflammatory macrophages. Here, we show that HMGB1 induces leukotriene production through a RAGE-dependent pathway, while HMGB1 plus C1q induces specialized proresolving lipid mediators lipoxin A4, resolvin D1, and resolvin D2 through a RAGE- and LAIR-1–dependent pathway. Leukotriene exposure contributes to induction of IRF5 in a positive-feedback loop. In contrast, resolvins (at 20 nM) block IRF5 induction and prevent the differentiation of inflammatory macrophages. Finally, we have generated a molecular mimic of HMGB1 plus C1q, which cross-links RAGE and LAIR-1 and polarizes monocytes to an antiinflammatory phenotype. These findings may provide a mechanism to control nonresolving inflammation in many pathologic conditions.

APA, Harvard, Vancouver, ISO, and other styles

Journal articles on the topic 'Lipid Mediators of Inflammation (LMI)'

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles