scholarly journals Lipoxin A4: a novel anti-inflammatory molecule?

Thorax ◽  
1995 ◽  
Vol 50 (2) ◽  
pp. 111-112 ◽  
Author(s):  
T H Lee
Keyword(s):  
Lipoxin A4 ◽  
Inflammatory Molecule ◽  
Anti Inflammatory

CCN2 Functions as Anti-Inflammatory Molecule in the Intervertebral Disc

2014 ◽  
Vol 4 (1_suppl) ◽  
pp. s-0034-1376756-s-0034-1376756
Author(s):  
Makarand V. Risbud
Keyword(s):  
Intervertebral Disc ◽  
Inflammatory Molecule ◽  
Anti Inflammatory

scholarly journals Could Lipoxins Represent a New Standard in Ischemic Stroke Treatment?

2021 ◽  
Vol 22 (8) ◽  
pp. 4207
Author(s):  
Nikola Tułowiecka ◽  
Dariusz Kotlęga ◽  
Andrzej Bohatyrewicz ◽  
Małgorzata Szczuko
Keyword(s):  
Ischemic Stroke ◽  
Cardiovascular Diseases ◽  
Blood Brain Barrier ◽  
Inflammatory Cytokines ◽  
The Body ◽  
Brain Barrier ◽  
Lipoxin A4 ◽  
Stroke Treatment ◽  
Blood Brain ◽  
Anti Inflammatory

Introduction: Cardiovascular diseases including stroke are one of the most common causes of death. Their main cause is atherosclerosis and chronic inflammation in the body. An ischemic stroke may occur as a result of the rupture of unstable atherosclerotic plaque. Cardiovascular diseases are associated with uncontrolled inflammation. The inflammatory reaction produces chemical mediators that stimulate the resolution of inflammation. One of these mediators is lipoxins—pro-resolving mediators that are derived from the omega-6 fatty acid family, promoting inflammation relief and supporting tissue regeneration. Aim: The aim of the study was to review the available literature on the therapeutic potential of lipoxins in the context of ischemic stroke. Material and Methods: Articles published up to 31 January 2021 were included in the review. The literature was searched on the basis of PubMed and Embase in terms of the entries: ‘stroke and lipoxin’ and ‘stroke and atherosclerosis’, resulting in over 110 articles in total. Studies that were not in full-text English, letters to the editor, and conference abstracts were excluded. Results: In animal studies, the injection/administration of lipoxin A4 improved the integrity of the blood–brain barrier (BBB), decreased the volume of damage caused by ischemic stroke, and decreased brain edema. In addition, lipoxin A4 inhibited the infiltration of neutrophils and the production of cytokines and pro-inflammatory chemokines, such as interleukin (Il-1β, Il-6, Il-8) and tumor necrosis factor-α (TNF-α). The beneficial effects were also observed after introducing the administration of lipoxin A4 analog—BML-111. BML-111 significantly reduces the size of a stroke and protects the cerebral cortex, possibly by reducing the permeability of the blood–brain barrier. Moreover, more potent than lipoxin A4, it has an anti-inflammatory effect by inhibiting the production of pro-inflammatory cytokines and increasing the amount of anti-inflammatory cytokines. Conclusions: Lipoxins and their analogues may find application in reducing damage caused by stroke and improving the prognosis of patients after ischemic stroke.

Preeclampsia is associated with a deficiency of lipoxin A4, an endogenous anti-inflammatory mediator

2014 ◽  
Vol 102 (1) ◽  
pp. 282-290.e4 ◽  
Author(s):  
Zhangye Xu ◽  
Feng Zhao ◽  
Feng Lin ◽  
Huiqiu Xiang ◽  
Ni Wang ◽  
...  
Keyword(s):  
Inflammatory Mediator ◽  
Lipoxin A4 ◽  
Anti Inflammatory

scholarly journals Endogenous lipid- and peptide-derived anti-inflammatory pathways generated with glucocorticoid and aspirin treatment activate the lipoxin A4 receptor

10.1038/nm786 ◽  
2002 ◽  
Vol 8 (11) ◽  
pp. 1296-1302 ◽  
Author(s):  
Mauro Perretti ◽  
Nan Chiang ◽  
Mylinh La ◽  
Iolanda M. Fierro ◽  
Stefano Marullo ◽  
...  
Keyword(s):  
Lipoxin A4 ◽  
Inflammatory Pathways ◽  
Endogenous Lipid ◽  
Anti Inflammatory

scholarly journals Dysregulation of prostaglandins, leukotrienes and lipoxin A4 in bronchiectasis

Thorax ◽  
2021 ◽  
pp. thoraxjnl-2020-216475
Author(s):  
Pallavi Bedi ◽  
Kerstin Ziegler ◽  
Phil D Whitfield ◽  
Donald Davidson ◽  
Adriano Giorgio Rossi ◽  
...  
Keyword(s):  
Healthy Volunteers ◽  
Severe Disease ◽  
Stable State ◽  
Lavage Fluid ◽  
Forced Expiratory Volume ◽  
Lipid Mediators ◽  
Prostaglandin E ◽  
Lipoxin A4 ◽  
Bacterial Killing ◽  
Anti Inflammatory

IntroductionBronchiectasis is characterised by excessive neutrophilic inflammation. Lipid mediators such as prostaglandins and leukotrienes have crucial roles in the inflammatory response. Further characterisation of these lipids and understanding the interplay of anti-inflammatory and proinflammatory lipid mediators could lead to the development of novel anti-inflammatory therapies for bronchiectasis.AimThe aim of our study was to characterise the lipids obtained from serum and airways in patients with bronchiectasis in the stable state.MethodsSix healthy volunteers, 10 patients with mild bronchiectasis, 15 with moderate bronchiectasis and 9 with severe bronchiectasis were recruited. All participants had 60 mL of blood taken and underwent a bronchoscopy while in the stable state. Lipidomics was done on serum and bronchoalveolar lavage fluid (BALF).ResultsIn the stable state, in serum there were significantly higher levels of prostaglandin E2 (PGE2), 15-hydroxyeicosatetranoic acid (15-HETE) and leukotriene B4 (LTB4) in patients with moderate–severe disease compared with healthy volunteers. There was a significantly lower level of lipoxin A4 (LXA4) in severe bronchiectasis.In BALF, there were significantly higher levels of PGE2, 5-HETE, 15-HETE, 9-hydroxyoctadecadienoic acid and LTB4 in moderate–severe patients compared with healthy volunteers.In the stable state, there was a negative correlation of PGE2 and LTB4 with % predicted forced expiratory volume in 1 s and a positive correlation with antibiotic courses.LXA4 improved blood and airway neutrophil phagocytosis and bacterial killing in patients with bronchiectasis. Additionally LXA4 reduced neutrophil activation and degranulation.ConclusionThere is a dysregulation of lipid mediators in bronchiectasis with excess proinflammatory lipids. LXA4 improves the function of reprogrammed neutrophils. The therapeutic efficacy of LXA4 in bronchiectasis warrants further studies.

scholarly journals Chemerin receptors (version 2019.4) in the IUPHAR/BPS Guide to Pharmacology Database

2019 ◽  
Vol 2019 (4) ◽  
Author(s):  
Anthony P. Davenport ◽  
Amy E. Monaghan
Keyword(s):  
Family Member ◽  
Orphan Receptor ◽  
Resolvin D1 ◽  
Endogenous Ligand ◽  
Lipoxin A4 ◽  
Founding Family ◽  
Sequential Metabolism ◽  
Anti Inflammatory

Nomenclature for the chemerin receptors is presented as recommended by NC-IUPHAR [14, 41]). The chemoattractant protein and adipokine, chemerin, has been shown to be the endogenous ligand for both chemerin family receptors. Chemerin1 was the founding family member, and when GPR1 was de-orphanised it was re-named Chermerin2 [41]. Chemerin1 is also activated by the lipid-derived, anti-inflammatory ligand resolvin E1 (RvE1), which is formed via the sequential metabolism of EPA by aspirin-modified cyclooxygenase and lipoxygenase [2, 3]. In addition, two GPCRs for resolvin D1 (RvD1) have been identified: FPR2/ALX, the lipoxin A4 receptor, and GPR32, an orphan receptor [43].

scholarly journals Downregulation of TNF-α/TNF-R1 Signals by AT-Lipoxin A4 May Be a Significant Mechanism of Attenuation in SAP-Associated Lung Injury

2019 ◽  
Vol 2019 ◽  
pp. 1-13 ◽  
Author(s):  
Suhui Yu ◽  
Jianming Xie ◽  
Yukai Xiang ◽  
Shengjie Dai ◽  
Dinglai Yu ◽  
...  
Keyword(s):  
Lung Injury ◽  
Tumor Necrosis Factor Receptor ◽  
Microvascular Endothelial Cell ◽  
Death Domain ◽  
Lipoxin A4 ◽  
Proinflammatory Mediators ◽  
Anti Inflammatory ◽  
Significant Mechanism

Our previous studies verified the potent anti-inflammatory effects against severe acute pancreatitis (SAP) of AT-Lipoxin A4 and their analogues. However, the anti-inflammatory effects of AT-Lipoxin A4 on SAP-associated lung injury are not thoroughly known. We used western blot, polymerase chain reaction (PCR), and immunofluorescence to investigate the downregulation of TNF-α signals in cellular and animal models of SAP-associated lung injury following AT-Lipoxin A4 intervention. In vitro, we found that AT-Lipoxin A4 markedly suppressed protein expression in TNF-α signals in human pulmonary microvascular endothelial cell, such as tumor necrosis factor receptor-associated factor 2 (TRAF2), TNF-R1-associated death domain (TRADD), receptor-interacting protein (RIP), vascular cell adhesion molecule-1 (VCAM-1), and E-selectin. Moreover, AT-Lipoxin A4 inhibited downstream signals activated by TNF-α, including NF-κB/p65, JNK/MAPK, and ERK/MAPK. In vivo, AT-Lipoxin A4 significantly decreased pathological scores of the pancreas and lungs and the serum levels of IL-6 and TNF-α. Immunofluorescence, western blotting, and real-time PCR assay showed that AT-Lipoxin A4 significantly attenuated the expression of TNF-R1, TRADD, TRAF2, and RIP in the lungs of SAP rats. In addition, the activation of NF-κB was also downregulated by AT-Lipoxin A4 administration as compared with SAP rats. AT-Lipoxin A4 could inhibit the production of proinflammatory mediators and activation of TNF-α downstream signals such as NF-κB and MAPK. Downregulation of TNF-α signals by AT-Lipoxin A4 may be a significant mechanism in the attenuation of SAP-associated lung injury.

Inhibition of secretory phospholipase A2 enzyme by bilirubin: A new role as endogenous anti-inflammatory molecule

2005 ◽  
Vol 276 (1-2) ◽  
pp. 219-225 ◽  
Author(s):  
Noor Mohamed Jameel ◽  
Brigitte M. Frey ◽  
Felix J. Frey ◽  
T. Veerabasappa Gowda ◽  
Bannikuppe S. Vishwanath
Keyword(s):  
Phospholipase A2 ◽  
Secretory Phospholipase A2 ◽  
Secretory Phospholipase ◽  
Inflammatory Molecule ◽  
Anti Inflammatory
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