Induction of Cytokine Expression in Leukocytes by Binding of Thrombin-Stimulated Platelets

Neumann, Franz‐Josef; Marx, Nikolaus; Gawaz, Meinrad; Brand, Korbinian; Ott, Ilka; Rokitta, Claudia; Sticherling, Christian; Meinl, Christian; May, Andreas E.; Schömig, Albert

doi:10.1161/01.cir.95.10.2387

Cited by 355 publications

(242 citation statements)

References 43 publications

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“…A functional soluble form of CD40L has recently been reported (39,40), suggesting that platelets may stimulate MC through either soluble or cell-surface CD40L. In contrast to data obtained in other cell types (11,12), blockade of P-selectin on platelets did not decrease MCP-1 production in coculture. Although we used doses of the anti-P-selectin mAb that can be expected to almost completely block surfaceexpressed P-selectin, mesangial production of MCP-1 was not significantly decreased.…”

Section: Discussionmentioning

confidence: 74%

“…Accordingly in our previous study, which examined the interaction between monocytes and MC, both cell-to-cell contact and soluble factors were required for the maximum activation of the latter (18). Other studies have shown that platelet contact induces chemokine or adhesion molecule expression by endothelial cells or leukocytes through NF-B activation (10,12). NF-B plays a critical role in inflammatory response through induction of a variety of proinflammatory genes.…”

Section: Discussionmentioning

confidence: 99%

“…P-selectin plays a crucial role in leukocyte or endothelial cell activation by platelet binding (11,12), and ␤1-integrins are implicated in platelet interactions with extracellular matrix (30). Activated platelets also express surface CD40L through which platelets can induce proinflammatory responses by endothelial cells (13).…”

Section: Cd40/cd40l Pathway Is Involved In Platelet-mediated Mcp-1 Prmentioning

confidence: 99%

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Human Platelets Stimulate Mesangial Cells to Produce Monocyte Chemoattractant Protein-1 via the CD40/CD40 Ligand Pathway and May Amplify Glomerular Injury

Tanaka

Kuroiwa²,

Ikeuchi³

et al. 2002

Journal of the American Society of Nephrology

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Abstract. Platelets are thought to play an important role in the initiation and the progression of a variety of glomerulonephritides. This study examined whether platelets induce production of monocyte chemoattractant protein-1 (MCP-1), a chemokine involved in leukocyte recruitment and glomerular injury, by cultured human mesangial cells (MC). To this end, platelets isolated from normal human donors were cocultured with MC at various ratios. MCP-1 synthesis was evaluated by quantitative real-time PCR and enzyme-linked immunosorbent assay. Platelets at 1:100 ratio (MC to platelets) induced an approximately 20-fold increase in mesangial MCP-1 mRNA and protein expression through an obligatory cell-to-cell contact-dependent mechanism. Importantly, blockade of the CD40/CD40 ligand (CD40L) pathway with neutralizing antibodies decreased MCP-1 production by approximately 60%. It was confirmed that CD40 was functionally expressed on MC. Gelshift assays and inhibitors of phosphorylation were used to demonstrate that activation of p38 mitogen-activated protein kinase, protein tyrosine kinases, and nuclear factor-B activation were essential for MCP-1 production. These data indicate that platelet/MC contact stimulates the production of MCP-1 and may contribute to glomerular inflammatory responses by recruiting leukocytes from the peripheral blood.

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Section: Discussionmentioning

confidence: 74%

Section: Discussionmentioning

confidence: 99%

Section: Cd40/cd40l Pathway Is Involved In Platelet-mediated Mcp-1 Prmentioning

confidence: 99%

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Human Platelets Stimulate Mesangial Cells to Produce Monocyte Chemoattractant Protein-1 via the CD40/CD40 Ligand Pathway and May Amplify Glomerular Injury

Tanaka

Kuroiwa²,

Ikeuchi³

et al. 2002

Journal of the American Society of Nephrology

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“…Similar processes occur in patients with COPD (Ferroni et al, 2000), atherosclerosis (Arber et al, 1991;Ott et al, 1996;Neumann et al, 1997;Sarma et al, 2002;Huo et al, 2003) and RA (Joseph et al, 2001;Bunescu et al, 2004). In this regard, experimental models of disease have provided evidence for a requirement of platelets in pulmonary eosinophil and lymphocyte recruitment in rabbits, guineapigs and mice in models of allergic inflammation (LellouchTubiana et al, 1988;Coyle et al, 1990;Pitchford et al, 2003Pitchford et al, , 2005; and neutrophil and monocyte recruitment in atherosclerosis (Arber et al, 1991;Neumann et al, 1997;Hayward et al, 1999) and RA (Schmitt-Sody et al, 2005). This phenomenon requires intact platelets expressing mediators on the cell surface, and in common with the occurrence of leukocyte recruitment in inflammatory diseases, platelet Pselectin is of particular importance (Diacovo et al, 1996a, b;Schober et al, 2002;Huo et al, 2003;Pitchford et al, 2005).…”

Section: Leukocyte Recruitment and Activation: Influence Of Plateletsmentioning

confidence: 77%

“…For example, studies with un-separated leukocyte populations reveal a significant increase in platelet-leukocyte complexes in allergic mice and in human asthmatics (Pitchford et al, 2003(Pitchford et al, , 2005. Similar processes occur in patients with COPD (Ferroni et al, 2000), atherosclerosis (Arber et al, 1991;Ott et al, 1996;Neumann et al, 1997;Sarma et al, 2002;Huo et al, 2003) and RA (Joseph et al, 2001;Bunescu et al, 2004). In this regard, experimental models of disease have provided evidence for a requirement of platelets in pulmonary eosinophil and lymphocyte recruitment in rabbits, guineapigs and mice in models of allergic inflammation (LellouchTubiana et al, 1988;Coyle et al, 1990;Pitchford et al, 2003Pitchford et al, , 2005; and neutrophil and monocyte recruitment in atherosclerosis (Arber et al, 1991;Neumann et al, 1997;Hayward et al, 1999) and RA (Schmitt-Sody et al, 2005).…”

Section: Leukocyte Recruitment and Activation: Influence Of Plateletsmentioning

confidence: 96%

Novel uses for anti‐platelet agents as anti‐inflammatory drugs

Pitchford

2007

British J Pharmacology

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An alteration in the character and function of platelets is manifested in patients with inflammatory diseases, and these alterations have been dissociated from the well‐characterized involvement of platelets in thrombosis and haemostasis. Recent evidence reveals platelet activation is sometimes critical in the development of inflammation. The mechanisms by which platelets participate in inflammation are diverse, and offer numerous opportunities for future drug intervention. There is now acceptance that platelets act as innate inflammatory cells in immune responses, with roles as sentinel cells undergoing surveillance, responding to microbial invasion, orchestrating leukocyte recruitment, and migrating through tissue, causing damage and influencing repair processes in chronic disease. Some of these processes are targeted by drugs that are being developed to target platelet participation in atherosclerosis. The actions of platelets therefore influence the pathogenesis of diverse inflammatory diseases in various body compartments, encompassing parasitic and bacterial infection, allergic inflammation (especially asthma and rhinitis), and non‐atopic inflammatory conditions, for example, chronic obstructive pulmonary disease (COPD), rheumatoid arthritis (RA), inflammatory bowel disease (IBD) and atherosclerosis. This review will first discuss the evidence for platelet activation in these various inflammatory diseases, and secondly discuss the mechanisms by which this pathogenesis occurs and the various anti‐platelet agents which have been developed to combat platelet activation in atherosclerosis and their potential future use for the treatment of other inflammatory diseases.British Journal of Pharmacology (2007) 152, 987–1002; doi:10.1038/sj.bjp.0707364; published online 2 July 2007

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Immunologic Aspects of Vasculitis and Cardiovascular Disease

Ledford¹

1997

JAMA

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The immunologic cardiovascular diseases are a heterogeneous group of conditions. Many of these entities are associated with serious morbidity and mortality resulting from cardiac impairment, ischemic complications, or organ dysfunction, particularly of the kidneys, lung, and nervous system. The systemic nature of these conditions, coupled with vague symptoms and nonspecific initial physical findings, makes the differential diagnosis complicated. Research has identified specific mediators and primary origins in some conditions, with infections often being responsible. Immunosuppressive therapy, despite the potential complications, has improved the prognosis of some of the more serious immunologic cardiovascular diseases. Improvement in the treatment of immunologic cardiovascular diseases awaits identification of additional causes, improved definition of host factors that predispose an individual to develop these conditions, and better understanding of the immune dysregulation responsible for the progression of disease. The potential pathophysiologic role of immunologic mechanisms in common disorders such as congestive heart failure and atherosclerosis is intriguing and offers the possibility of novel therapies in these prevalent conditions.

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Induction of Cytokine Expression in Leukocytes by Binding of Thrombin-Stimulated Platelets

Abstract: In patients with AMI, leukocyte-platelet adhesion is increased. Binding of activated platelets induces IL-1 beta, IL-8, and MCP-1 in leukocytes. Our findings suggest that leukocyte-platelet adhesion contributes to the regulation of inflammatory responses in AMI.

Cited by 355 publications

References 43 publications

Human Platelets Stimulate Mesangial Cells to Produce Monocyte Chemoattractant Protein-1 via the CD40/CD40 Ligand Pathway and May Amplify Glomerular Injury

Human Platelets Stimulate Mesangial Cells to Produce Monocyte Chemoattractant Protein-1 via the CD40/CD40 Ligand Pathway and May Amplify Glomerular Injury

Novel uses for anti‐platelet agents as anti‐inflammatory drugs

Immunologic Aspects of Vasculitis and Cardiovascular Disease

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