Platelets and inflammation

Klinger, Matthias

doi:10.1007/s004290050075

Cited by 183 publications

(139 citation statements)

References 91 publications

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“…An alternate source for many of these, or similar mediators is the platelet. Platelets are anucleate cellular fragments containing ␣ granules and dense granules that, upon stimulation, can release a variety of mediators capable of inducing vascular permeability and leukocyte recruitment (37). In this study, we demonstrated that the allergeninduced, mast cell-independent increase in vascular permeability could be abrograted by the depletion of circulating platelets (Ͼ99%), confirming that this cell fragment is an important pool for a mediator of vascular permeability.…”

Section: Discussionsupporting

confidence: 61%

Mast Cell-Independent Mechanisms of Immediate Hypersensitivity: A Role for Platelets

Cara

Ebbert

McCafferty

2004

The Journal of Immunology

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Mast cells have been implicated as the central effectors in allergic responses, yet a fatal anaphylactic response can be induced in mast cell-deficient mice. In this study, we examined the immediate hypersensitivity response in wild-type (WT) and mast cell-deficient mice (W/Wv) in two different tissues (skin and skeletal muscle). Vascular permeability and leukocyte recruitment were studied after immediate challenge or 4 h postchallenge in OVA-sensitized mice. In skin, immediate challenge induced a significant increase in vascular permeability (75%) within 30 min and was accompanied by increased leukocyte adhesion 4 h postchallenge. In the absence of mast cells, no changes in vascular permeability or leukocyte recruitment were observed in skin. In WT skeletal muscle, immediate challenge induced a rapid increase (80%) in vascular permeability within 5 min and significant leukocyte recruitment after 4 h. Surprisingly, in W/Wv, a gradual increase in vascular permeability was observed, reaching a maximum (50%) within 30 min. Despite the absence of mast cells, subsequent leukocyte emigration was similar to that observed in WT mice. Pretreatment with anti-platelet serum in W/Wv returned Ag-induced vascular permeability and leukocyte recruitment to baseline. Platelets were shown to interact with endothelium in skeletal muscle, but not dermal microvasculature. These data illustrate that mast cells play a prominent role in vascular permeability and leukocyte recruitment in skin in response to Ag, however, in skeletal muscle; these changes can occur in the absence of mast cells, and are mediated, in part, by the presence of platelets.

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Section: Discussionsupporting

confidence: 61%

Mast Cell-Independent Mechanisms of Immediate Hypersensitivity: A Role for Platelets

Cara

Ebbert

McCafferty

2004

The Journal of Immunology

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“…These interactions potentially induce platelet activation. Normally, non-activated platelets store CD62P in the alpha-granule membranes, but several stimulators rapidly translocate to the platelet surface (30)(31)(32)(33). Platelet activated by these stimulators releases alpha-granule constituents, such as PF4 and growth factors (12,13).…”

Section: Discussionmentioning

confidence: 99%

Feasibility of improving platelet-rich plasma therapy by using chitosan with high platelet activation ability

Hattori

Ishihara

2017

Experimental and Therapeutic Medicine

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Abstract. Platelet-rich plasma (PRP) is blood plasma containing a high number of platelets that release growth factors for wound healing and tissue regeneration. In the present study, the feasibility of improving PRP therapy by using chitosan that exhibits high platelet activation ability was investigated. A total of 13 chitosan samples with different molecular weight (Mw) and degree of deacetylation (DDA) were individually added to blood samples of rats and the amount of growth factors, albumin and fibrinogen in plasma was measured. To examine the influence of plasma activated by chitosan on the proliferation of fibroblasts and adipose tissue-derived stromal cells (ASCs), the plasma was added to the culture medium of human fibroblasts and adipose tissue-derived stromal cells. Chitosan with a DDA of >75% increased the release of platelet factor 4 into the plasma. The amount of growth factors released into the plasma and platelet activation varied depending on the Mw and DDA, while albumin and fibrinogen were hardly affected. The proliferation rate was highest when using plasma activated by chitosan with a DDA of 75-85% and an Mw of 50,000-190,000 Da. These results suggested that the effectiveness of PRP therapy may be improved by using chitosan with a DDA of 75-85% and an Mw of 50,000-190,000 Da.

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“…This is a novel observation, considering that platelets have been long considered the major source of plasma sCD40L (40,50). This reversal in the predominant source of sCD40L is likely to be explained by the fact that platelets contain only preformed CD40L and lack synthetic capacity even after stimulation, whereas activated T cells can produce massive quantities of inflammatory molecules for prolonged periods of time (51). When infliximab was added to activated T cells, levels of sCD40L were significantly reduced, while platelet-derived sCD40L remained unchanged.…”

Section: Discussionmentioning

confidence: 99%

TNF-α Blockade Down-Regulates the CD40/CD40L Pathway in the Mucosal Microcirculation: A Novel Anti-Inflammatory Mechanism of Infliximab in Crohn’s Disease

Danese¹,

Sans

Scaldaferri³

et al. 2006

The Journal of Immunology

153

101

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The CD40/CD40 ligand (CD40L) pathway is involved in Crohn’s disease (CD) pathogenesis. In the patients’ circulation, soluble CD40L (sCD40L) levels are elevated and surface CD40L is increased in platelets and T cells, whereas in the intestine CD40 is overexpressed in the microvasculature and CD40L in platelets and T cells. The therapeutic effects of infliximab in CD are attributed to its systemic anti-TNF-α action, but because TNF-α modulates both CD40 and CD40L, we investigated whether infliximab affects the CD40/CD40L pathway in the intestine. Eighteen CD patients were evaluated before and after infliximab therapy. Plasma sCD40L was measured by ELISA and platelet and peripheral blood T cell (PBT) CD40L expression by flow cytometry. Microvascular CD40 and VCAM-1 expression were assessed in mucosal biopsies by immunohistochemistry and by flow cytometry in human intestinal microvascular endothelial cells (HIMEC). Cell cultures were performed in the presence and absence of infliximab. Infliximab treatment significantly reduced plasma sCD40L levels and eliminated CD40 and VCAM-1 from mucosal microvessels. In vitro infliximab prevented TNF-α-induced CD40 and VCAM-1 expression by HIMEC, and reduced PBT, but not platelet, surface CD40L expression and sCD40L release. In addition, infliximab decreased T cell-induced VCAM-1 expression in HIMEC by down-regulating CD40L in T cells and promoting T cells apoptosis. These findings point to a novel mechanism of action of infliximab, i.e., the disruption of CD40/CD40L-dependent cognate interactions between intestinal microvessels and T cells. Thus, in addition to neutralizing TNF-α and inducing T cell death, the therapeutic effects of infliximab in CD appear to be also mediated by inhibition of vascular inflammation in the gut.

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Platelets and inflammation

Cited by 183 publications

References 91 publications

Mast Cell-Independent Mechanisms of Immediate Hypersensitivity: A Role for Platelets

Mast Cell-Independent Mechanisms of Immediate Hypersensitivity: A Role for Platelets

Feasibility of improving platelet-rich plasma therapy by using chitosan with high platelet activation ability

TNF-α Blockade Down-Regulates the CD40/CD40L Pathway in the Mucosal Microcirculation: A Novel Anti-Inflammatory Mechanism of Infliximab in Crohn’s Disease

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