Platelets Abrogate Leukotriene B4 Generation by Human Blood Neutrophils Stimulated with Monosodium Urate Monohydrate or f-Met-Leu-Phe In Vitro

Chabannes, B.; Poubelle, Patrice E.; Molière, Patrick; Médicis, Rinaldo de; Lussier, A; Lagarde, Michel

doi:10.1097/01.lab.0000062855.90029.d8

Cited by 3 publications

(3 citation statements)

References 57 publications

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“…The inhibitory factor can be adenosine as identified in ligand-operated interactions of platelets with neutrophils, but the platelet-derived product responsible for down regulation of neutrophil lipid mediators release and generation remains to be identified. This could have a significant impact on the homeostatic process of inflammation (Chabannes et al, 2003 ).…”

Section: Discussionmentioning

confidence: 99%

Analysis of the Effect of Intestinal Ischemia and Reperfusion on the Rat Neutrophils Proteome

Tahir

Arshid

Fontes

et al. 2018

Front. Mol. Biosci.

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Intestinal ischemia and reperfusion injury is a model system of possible consequences of severe trauma and surgery, which might result into tissue dysfunction and organ failure. Neutrophils contribute to the injuries preceded by ischemia and reperfusion. However, the mechanisms by which intestinal ischemia and reperfusion stimulate and activate circulating neutrophils is still not clear. In this work, we used proteomics approach to explore the underlying regulated mechanisms in Wistar rat neutrophils after ischemia and reperfusion. We isolated neutrophils from three different biological groups; control, sham laparotomy, and intestinal ischemia/reperfusion. In the workflow, we included iTRAQ-labeling quantification and peptide fractionation using HILIC prior to LC-MS/MS analysis. From proteomic analysis, we identified 2,045 proteins in total that were grouped into five different clusters based on their regulation trend between the experimental groups. A total of 417 proteins were found as significantly regulated in at least one of the analyzed conditions. Interestingly, the enzyme prediction analysis revealed that ischemia/reperfusion significantly reduced the relative abundance of most of the antioxidant and pro-survival molecules to cause more tissue damage and ROS production whereas some of the significantly up regulated enzymes were involved in cytoskeletal rearrangement, adhesion and migration. Clusters based KEGG pathways analysis revealed high motility, phagocytosis, directional migration, and activation of the cytoskeletal machinery in neutrophils after ischemia and reperfusion. Increased ROS production and decreased phagocytosis were experimentally validated by microscopy assays. Taken together, our findings provide a characterization of the rat neutrophil response to intestinal ischemia and reperfusion and the possible mechanisms involved in the tissue injury by neutrophils after intestinal ischemia and reperfusion.

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Section: Discussionmentioning

confidence: 99%

Analysis of the Effect of Intestinal Ischemia and Reperfusion on the Rat Neutrophils Proteome

Tahir

Arshid

Fontes

et al. 2018

Front. Mol. Biosci.

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“…We speculate that platelets might present their CS to PMNL, and inhibition of LT synthesis may be a consequence of such a lipid exchange. Physiological concentrations of platelets inhibited LT biosynthesis in human neutrophils in an adhesion‐dependent manner [49,50]. After degranulation by thrombin under nonaggregating conditions, platelets lost their inhibitory activity [50].…”

Section: Discussionmentioning

confidence: 99%

Cholesterol and its anionic derivatives inhibit 5‐lipoxygenase activation in polymorphonuclear leukocytes and MonoMac6 cells

et al. 2006

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Mammalian 5-lipoxygenase (5-LO) converts arachidonic acid (AA) to 5-hydroperoxyeicosatetraenoic acid (5-HPETE) and further to leukotriene A4 (LTA4) [1]. This substance is a key intermediate in the biosynthesis of two leukotriene families that act as potent mediators of cell proliferation [2], apoptosis [3], tumorigenesis and inflammatory processes such as allergy, atherosclerosis and asthma [4,5]. 5-LO is activated by intracellular Ca 2+ influx that leads to translocation and binding of 5-LO to the nuclear membrane [6][7][8][9][10][11]. It is commonly observed that the N-terminal domain of the enzyme may function like the protein kinase C C2 domain and facilitates Ca 2+ -mediated membrane binding [12][13][14][15][16].There are two main physicochemical factors influencing translocation of 5-LO to the membrane. First, the calcium-ion binding counteracts electrostatic repulsion of anionic C2 domain of 5-LO at the surface of anionic membranes [15]. Secondly, it may be regulated by membrane surface charge and membrane lipids. It was shown that phosphatidyl choline (PC) head groups facilitate the 5-LO C2-like domain binding to membranes, and that Trp13, Trp75, Trp102 of 5-LO are involved in these protein-lipid interactions [15] 5-Lipoxygenase (5-LO) is the key enzyme in the biosynthesis of leukotrienes (LTs), biological mediators of host defense reactions and of inflammatory diseases. While the role of membrane binding in the regulation of 5-LO activity is well established, the effects of lipids on cellular activity when added to the medium has not been characterized. Here, we show such a novel function of the most abundant sulfated sterol in human blood, cholesterol sulfate (CS), to suppress LT production in human polymorphonuclear leukocytes (PMNL) and Mono Mac6 cells. We synthesized another anionic lipid, cholesterol phosphate, which demonstrated a similar capacity in suppression of LT synthesis in PMNL. Cholesteryl acetate was without effect. Cholesterol increased the effect of CS on 5-LO product synthesis. CS and cholesterol also inhibited arachidonic acid (AA) release from PMNL. Addition of exogenous AA increased the threshold concentration of CS required to inhibit LT synthesis. The effect of cholesterol and its anionic derivatives can arise from remodeling of the cell membrane, which interferes with 5-LO activation. The fact that cellular LT production is regulated by sulfated cholesterol highlights a possible regulatory role of sulfotransferases ⁄ sulfatases in 5-LO product synthesis.

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“…Lipoxins are metabolites in the arachidonic acid pathway, as described by Hamberg and Samuelsson [ 114 ], and are very potent anti-inflammatory molecules that play important roles in limiting pro-inflammatory neutrophil activation, preventing their migration into tissues, and in driving the resolution of inflammation [ 110 , 115 ]. It is important to note that platelets lack the ability to synthesize lipoxins without the LTs produced by neutrophils [ 116 ]. This switch from initial generation of pro-inflammatory lipid mediators into ultimately anti-inflammatory lipid mediators in neutrophils is thought to prevent further neutrophil recruitment and inflammatory activation while simultaneously activating resolution pathways that can accelerate tissue healing [ 117 ].…”

Section: Mimetic Properties Of Prp In Tissue Repairmentioning

confidence: 99%

Modifying Orthobiological PRP Therapies Are Imperative for the Advancement of Treatment Outcomes in Musculoskeletal Pathologies

et al. 2022

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Autologous biological cellular preparations have materialized as a growing area of medical advancement in interventional (orthopedic) practices and surgical interventions to provide an optimal tissue healing environment, particularly in tissues where standard healing is disrupted and repair and ultimately restoration of function is at risk. These cellular therapies are often referred to as orthobiologics and are derived from patient’s own tissues to prepare point of care platelet-rich plasma (PRP), bone marrow concentrate (BMC), and adipose tissue concentrate (ATC). Orthobiological preparations are biological materials comprised of a wide variety of cell populations, cytokines, growth factors, molecules, and signaling cells. They can modulate and influence many other resident cells after they have been administered in specific diseased microenvironments. Jointly, the various orthobiological cell preparations are proficient to counteract persistent inflammation, respond to catabolic reactions, and reinstate tissue homeostasis. Ultimately, precisely delivered orthobiologics with a proper dose and bioformulation will contribute to tissue repair. Progress has been made in understanding orthobiological technologies where the safety and relatively easy manipulation of orthobiological treatment tools has been demonstrated in clinical applications. Although more positive than negative patient outcome results have been registered in the literature, definitive and accepted standards to prepare specific cellular orthobiologics are still lacking. To promote significant and consistent clinical outcomes, we will present a review of methods for implementing dosing strategies, using bioformulations tailored to the pathoanatomic process of the tissue, and adopting variable preparation and injection volume policies. By optimizing the dose and specificity of orthobiologics, local cellular synergistic behavior will increase, potentially leading to better pain killing effects, effective immunomodulation, control of inflammation, and (neo) angiogenesis, ultimately contributing to functionally restored body movement patterns.

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Platelets Abrogate Leukotriene B4 Generation by Human Blood Neutrophils Stimulated with Monosodium Urate Monohydrate or f-Met-Leu-Phe In Vitro

Cited by 3 publications

References 57 publications

Analysis of the Effect of Intestinal Ischemia and Reperfusion on the Rat Neutrophils Proteome

Analysis of the Effect of Intestinal Ischemia and Reperfusion on the Rat Neutrophils Proteome

Cholesterol and its anionic derivatives inhibit 5‐lipoxygenase activation in polymorphonuclear leukocytes and MonoMac6 cells

Modifying Orthobiological PRP Therapies Are Imperative for the Advancement of Treatment Outcomes in Musculoskeletal Pathologies

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