Monocyte/Macrophage-Derived Microparticles Up-Regulate Inflammatory Mediator Synthesis by Human Airway Epithelial Cells

Cerri, Chiara; Chimenti, Daniele; Conti, Ilaria; Neri, Tommaso; Paggiaro, Pierluigi; Celi, Alessandro

doi:10.4049/jimmunol.177.3.1975

Cited by 96 publications

(83 citation statements)

References 18 publications

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“…18 Peripheral blood mononuclear cells were isolated from buffy coats by Ficoll TM (Lymphocyte separation medium 1077). Monocytes were isolated by CD14 + immuno-magnetic separation on magnetic sphere columns (Miltenyi Biotec, Bergish Gladbach, Germany).…”

Section: Generation Of Microparticles From Blood Cellsmentioning

confidence: 99%

Leukocyte- and endothelial-derived microparticles: a circulating source for fibrinolysis

et al. 2012

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The online version of this article has a Supplementary Appendix. BackgroundWe recently assigned a new fibrinolytic function to cell-derived microparticles in vitro. In this study we explored the relevance of this novel property of microparticles to the in vivo situation. Design and MethodsCirculating microparticles were isolated from the plasma of patients with thrombotic thrombocytopenic purpura or cardiovascular disease and from healthy subjects. Microparticles were also obtained from purified human blood cell subpopulations. The plasminogen activators on microparticles were identified by flow cytometry and enzyme-linked immunosorbent assays; their capacity to generate plasmin was quantified with a chromogenic assay and their fibrinolytic activity was determined by zymography. ResultsCirculating microparticles isolated from patients generate a range of plasmin activity at their surface. This property was related to a variable content of urokinase-type plasminogen activator and/or tissue plasminogen activator. Using distinct microparticle subpopulations, we demonstrated that plasmin is generated on endothelial and leukocyte microparticles, but not on microparticles of platelet or erythrocyte origin. Leukocyte-derived microparticles bear urokinase-type plasminogen activator and its receptor whereas endothelial microparticles carry tissue plasminogen activator and tissue plasminogen activator/inhibitor complexes. ConclusionsEndothelial and leukocyte microparticles, bearing respectively tissue plasminogen activator or urokinase-type plasminogen activator, support a part of the fibrinolytic activity in the circulation which is modulated in pathological settings. Awareness of this blood-borne fibrinolytic activity conveyed by microparticles provides a more comprehensive view of the role of microparticles in the hemostatic equilibrium.Key words: fibrinolytic microparticles, plasmin, plasminogen, uPA; tPA. Plawinski L, Robert S, Doeuvre L, Sabatier F, Martinez de Lizarrondo S, Mezzapesa A, Anfosso F, Leroyer AS, Poullin P, Jourde N, Njock M-S, Boulanger CM, Anglés-Cano E, and Dignat-George F. Leukocyte-and endothelial-derived microparticles: a circulating source for fibrinolysis. Haematologica 2012;97(12):1864-1872. doi:10.3324/haematol.2012 This is an open-access paper. Citation: Lacroix R, Leukocyte-and endothelial-derived microparticles: a circulating source for fibrinolysis ABSTRACT© F e r r a t a S t o r t i F o u n d a t i o n

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Section: Generation Of Microparticles From Blood Cellsmentioning

confidence: 99%

Leukocyte- and endothelial-derived microparticles: a circulating source for fibrinolysis

et al. 2012

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“…MMPs were derived from human peripheral blood monocytes by stimulation with 12 μM A23187 according to a previously published protocol (61). These were characterized by anti-CD14 and annexin V staining.…”

Section: Figurementioning

confidence: 99%

Platelet CD36 mediates interactions with endothelial cell–derived microparticles and contributes to thrombosis in mice

Li²,

et al. 2008

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CD36 is a scavenger receptor that binds multiple ligands, including phosphatidyl serine (PS). Although CD36 -mice do not have a bleeding diathesis, we show here that they do have significantly prolonged thrombotic occlusion times in response to FeCl 3 -induced vascular injury. Because cell-derived microparticles (MPs) are generated in response to vascular injury and circulate in patients with prothrombotic diseases, we hypothesized that PS exposed on their surfaces could be an endogenous CD36 ligand that transmits an activating signal to platelets. We found that MPs prepared from human ECs, monocytes, or platelets or isolated from blood of normal subjects bound to platelets. Binding was not observed with platelets from CD36 -donors and was inhibited by an anti-CD36 antibody or by blockade of exposed PS by annexin V or anti-PS IgM. Preincubation of platelets with MPs led to CD36-dependent augmentation of platelet activation in response to low doses of ADP, as assessed by measuring α 2b β 3 activation, P-selectin expression, and aggregation. Immunofluorescence confocal microscopy of murine carotid thrombi from CD36 -mice showed a significant decrement in endothelial antigen accumulation, which suggests that CD36 plays a role in MP recruitment into thrombi. These results provide what we believe to be a novel role for CD36 in thrombosis.

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“…We have previously demonstrated that stimulation of human monocytes/macrophages with the calcium ionophore, A23187, or with histamine, causes MP shedding, and that incubation of these MP with lung epithelial cells results in upregulation of proinflammatory mediator synthesis, including IL-8 and monocyte chemotactic protein (MCP)-1 [6]. IL-8 is a potent chemoattractant for neutrophils involved in the pathogenesis of the inflammatory response typical of chronic obstructive pulmonary disease (COPD).…”

mentioning

confidence: 99%

Role of NF- B and PPAR- in lung inflammation induced by monocyte-derived microparticles

Neri

Armani²,

Pegoli³

et al. 2010

European Respiratory Journal

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Microparticles (MP) are phospholipid vesicles shed by cells upon activation or apoptosis. Monocyte-derived MP upregulate the synthesis of proinflammatory mediators by lung epithelial cells; the molecular bases of such activity are unknown. Peroxisome proliferatoractivated receptors (PPAR) have been demonstrated to be involved in the modulation of nuclear factor (NF)-kB transcriptional activity and inflammation.We investigated whether the upregulation of the synthesis of proinflammatory cytokines by human lung epithelial cells induced by monocyte/macrophage-derived MP involves NF-kB activation and is modulated by PPAR-c.MP were generated by stimulation of human monocytes/macrophages with the calcium ionophore, A23187. MP were incubated with human lung epithelial cells. NF-kB translocation was assessed by electrophoretic mobility shift assay. Interleukin (IL)-8 and monocyte chemotactic protein (MCP)-1 synthesis was assessed by ELISA and RT-PCR.Stimulation of A549 alveolar cells with monocyte/macrophage-derived MP caused an increase in NF-kB activation and IL-8 and MCP-1 synthesis that was inhibited by pre-incubation with the PPAR-c agonists, rosiglitazone and 15-deoxy-D 12,14 -prostaglandin-J 2 . Parallel experiments with normal human bronchial epithelial cells largely confirmed the results. The effects of PPAR-c agonists were reversed by the specific antagonist, GW9662.Upregulation of the synthesis of proinflammatory mediators by human lung epithelial cells induced by monocyte/macrophage-derived MP is mediated by NF-kB activation through a PPAR-c dependent pathway.

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Monocyte/Macrophage-Derived Microparticles Up-Regulate Inflammatory Mediator Synthesis by Human Airway Epithelial Cells

Cited by 96 publications

References 18 publications

Leukocyte- and endothelial-derived microparticles: a circulating source for fibrinolysis

Leukocyte- and endothelial-derived microparticles: a circulating source for fibrinolysis

Platelet CD36 mediates interactions with endothelial cell–derived microparticles and contributes to thrombosis in mice

Role of NF- B and PPAR- in lung inflammation induced by monocyte-derived microparticles

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