Endotoxin-mediated inhibition of human platelet aggregation

Saba, Hussain I.; Saba, Sabiha R.; Morelli, Genevieve A.; Hartmann, Robert C.

doi:10.1016/0049-3848(84)90103-8

Cited by 42 publications

(20 citation statements)

References 15 publications

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“…A TLR4/MyD88-dependent activating pathway involving cyclic GMP, protein kinase G, and nitric oxide synthase has also been described, and it was suggested that this mechanism can inhibit or activate platelets depending on the concentrations of LPS 58 . This might explain inhibition of platelet activities by LPS in some earlier reports 61, 62 . Taken together, the studies reported to date suggest that there are gaps in our understanding of signaling cascades triggered by platelet TLR4, and that novel pathways may be involved.…”

Section: The Inflammatory Repertoire Of Plateletsmentioning

confidence: 55%

Platelets as Cellular Effectors of Inflammation in Vascular Diseases

Rondina

Weyrich

Zimmerman

2013

Circulation Research

264

310

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Platelets are chief effector cells in hemostasis. In addition, they are multifaceted inflammatory cells with functions that span the continuum from innate immune responses to adaptive immunity. Activated platelets have key “thromboinflammatory” activities in a variety of vascular disorders and vasculopathies. Recently-identified inflammatory and immune activities provide insights into the biology of these versatile blood cells that are directly relevant to human vascular diseases.

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Section: The Inflammatory Repertoire Of Plateletsmentioning

confidence: 55%

Platelets as Cellular Effectors of Inflammation in Vascular Diseases

Rondina

Weyrich

Zimmerman

2013

Circulation Research

264

310

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“…The effects of bacterial products on platelet function have been inconsistent and appear to vary according to species, timing of the study, and pathogenesis of the sepsis [78]. For example, LPS has been shown to increase platelet aggregation in various animal models [79,80], yet bacterial products seem to decrease human platelet aggregation in vitro [81,82]. It has, however, become increasingly apparent that platelets play a complex role in sepsis.…”

Section: Sepsismentioning

confidence: 99%

Platelets and innate immunity

Semple

Freedman

2009

Cell. Mol. Life Sci.

279

231

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Although platelets are best known as primary mediators of hemostasis, this function intimately associates them with inflammatory processes, and it has been increasingly recognized that platelets play an active role in both innate and adaptive immunity. For example, platelet adhesive interactions with leukocytes and endothelial cells via P-selectin can lead to several pro-inflammatory events, including leukocyte rolling and activation, production of cytokine cascades, and recruitment of the leukocytes to sites of tissue damage. Superimposed on this, platelets express immunologically-related molecules such as CD40L and Toll-like receptors that have been shown to functionally modulate innate immunity. Furthermore, platelets themselves can interact with microorganisms, and several viruses have been shown to cross-react immunologically with platelet antigens. This review discusses the central role that platelets play in inflammation, linking them with varied pathological conditions, such as atherosclerosis, sepsis, and immune thrombocytopenic purpura, and suggests that platelets also act as primary mediators of our innate defences.

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“…More recently, LPS in vitro was shown to increase thrombin-and collagen-induced platelet aggregation, and to stimulate platelet secretion of dense and alpha granule (Zhang et al, 2009). In contrast, LPS in vitro has been shown to inhibit platelet aggregation induced by ionophore A23187 and collagen (Saba et al, 1984;Sheu et al, 1998Sheu et al, , 1999. In addition, LPS reduces Ca 2+ mobilization and thromboxane A 2 formation in platelets, and augments the nitric oxide (NO)/cGMP levels (Sheu et al, 1998(Sheu et al, , 1999.…”

Section: Introductionmentioning

confidence: 99%