Density‐dependent induction of TNF‐α release from human monocytes by immobilized P‐selectin

Koike, Junzo; Nagata, Kisaburo; Kudo, Sanae; Tsuji, Tsutomu; Irimura, Tatsuro

doi:10.1016/s0014-5793(00)01765-8

Cited by 36 publications

(24 citation statements)

References 27 publications

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“…Another anti-P-selectin Ab (2D7, IgG1) [13] was purified from conditioned medium of hybridoma in our laboratory. For purification of P-selectin, mAb 2D7 was conjugated to CNBr-activated Sepharose 4B (GE Healthcare) according to the manufacturer’s instructions.…”

Section: Methodsmentioning

confidence: 99%

“…The antibody (Ab) engagement of PSGL-1 upregulates the expression of colony-stimulating factor (CSF)-1 mRNA in Jurkat leukemic cells [12]. Our previous study also demonstrated that P-selectin immobilized on a culture plate effectively induced monocytes to secrete tumor necrosis factor (TNF)-α [13]. Cytokines secreted from monocytes have been shown to regulate various types of immune responses and inflammatory/allergic diseases.…”

Section: Introductionmentioning

confidence: 99%

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Cytokine Secretion from Human Monocytes Potentiated by P-Selectin-Mediated Cell Adhesion

Suzuki

Hamada

Shodai

et al. 2012

Int Arch Allergy Immunol

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Background/Aim: P-selectin is a carbohydrate-recognizing cell adhesion molecule expressed on activated platelets and endothelial cells. It plays a crucial role in the recruitment of leukocytes to inflammatory and hemorrhagic sites. Cell adhesion mediated by P-selectin induces leukocyte activation, such as the generation of reactive oxygen species and the expression of blood coagulation factors. We assessed how P-selectin-mediated cell adhesion affects cytokine secretion from monocytes. Methods: Human peripheral blood monocytes were cultured in a plate that had been coated with P-selectin purified from human platelets, and cytokines released in the culture supernatant from monocytes were determined by ELISA. Results: The secretion of tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6, IL-8, IL-12 and macrophage inflammatory protein-1β increased 3- to 10-fold in response to P-selectin compared with unstimulated monocytes. We next examined the effects of cytokine treatment of monocytes on their susceptibility to P-selectin. The secretion of TNF-α from monocytes in response to P-selectin was increased when monocytes were preincubated with granulocyte/macrophage colony-stimulating factor, monocyte chemotactic protein-1 or interferon-γ (IFN-γ); IFN-γ was the most effective in potentiating TNF-α secretion from monocytes. Conclusion: These results suggest that the interaction of monocytes with P-selectin plays an important role not only in their trafficking but also in the regulation of cytokine production by these cells.

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Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Cytokine Secretion from Human Monocytes Potentiated by P-Selectin-Mediated Cell Adhesion

Suzuki

Hamada

Shodai

et al. 2012

Int Arch Allergy Immunol

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“…We believe that because our experiments are performed in a plateletfree environment might be one reason for this observation, because P-selectin, which can be found on the surface of activated platelets, has been identified as a relevant inducer of TNF-␣ release from monocytes. 42 A recent publication assigns platelets a relevant role in TRALI induced by monoclonal antibodies against MHC I in a murine model. 43 It is conceivable that further monocyte activation by platelets might trigger TRALI under certain conditions in vivo.…”

Section: Hla Class II Antibody-inducedmentioning

confidence: 99%

Mechanism of transfusion-related acute lung injury induced by HLA class II antibodies

Sachs

Wasel

Bayat

et al. 2011

Blood

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Transfusion-related acute lung injury (TRALI) is the leading cause of transfusion-associated mortality in the United States and other countries. In most TRALI cases, human leukocyte antigen (HLA) class II antibodies are detected in implicated donors. However, the corresponding antigens are not present on the cellular key players in TRALI: neutrophils and endothelium. In this study, we identify monocytes as a primary target in HLA class II-induced TRALI. Monocytes become activated when incubated with matched HLA class II antibodies and are capable of activating neutrophils, which, in turn, can induce disturbance of an endothelial barrier. In an ex vivo rodent model, HLA class II antibody-dependent monocyte activation leads to severe pulmonary edema in a relevant period of time, whenever neutrophils are present and the endothelium is preactivated. Our data suggest that in most TRALI cases, monocytes are cellular key players, because HLA class II antibodies induce TRALI by a reaction cascade initiated by monocyte activation. Furthermore, our data support the previous assumption that TRALI pathogenesis follows a threshold model. Having identified the biologic mechanism of HLA class II antibodyinduced TRALI, strategies to avoid plasma from immunized donors, such as women with a history of pregnancy, appear to be justified preventive measures. (Blood. 2011;117(2):669-677) IntroductionTransfusion-related acute lung injury (TRALI) is the leading cause of transfusion-associated death in the United States and other countries. 1 It typically presents within 6 hours after transfusion as a clinical syndrome characterized by acute respiratory distress, hypoxemia, and a bilateral pulmonary edema on chest x-ray. 2 The incidence of TRALI has been estimated as 1/5000 for all blood components, and current mortality rates are in the range of 5%-25%. 3 All blood components have been implicated in TRALI, but those containing large amounts of plasma are mainly responsible. [3][4][5] A recently published literature review states that in 80% of all TRALI cases, white blood cell antibodies can be identified in the implicated blood donor, 6 and most implicated donors have been women with a history of pregnancy. Pregnancy results in alloimmunization against paternal white blood cell antigens in 21%-24% of women, 7,8 with 3 main antibody specificities: human leukocyte antigen (HLA) class I, HLA class II, and human neutrophil antigens (HNAs).The capability of antibodies recognizing either HNA 9-11 or HLA class I 12,13 to precipitate TRALI has been proved in different animal models. It is consensus opinion that neutrophil activation is the key mechanism by which antibodies to HNA and to HLA class I mediate TRALI, 4,14 be it by direct binding to the cognate antigen on the surface of the neutrophil [9][10][11]13 or, in the case of HLA class I antibodies, possibly by binding to HLA class I molecules on pulmonary endothelial cells, which leads to neutrophil trapping by the neutrophils' Fc receptors and subsequent neutrophil activation by receptor...

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“…37 Similarly, one possibility is that the P-selectininduced phosphatidylserine exposure is not a direct effect of signaling through ligated PSGL-1, but rather the effect of mediators (eg, tumor necrosis factor-␣) released by the monocyte when stimulated with P-selectin. 10 The small amount of phosphatidylserine expression on THP-1 cells incubated with unstimulated platelets very likely resulted from a slight degree of activation of the platelets that occurred during their preparation. This interpretation is supported by the observation that an anti-PSGL-1 antibody reduced phosphatidylserine exposure in the cells incubated with activated platelets to levels below those observed in THP-1 cells incubated with unstimulated platelets.…”

Section: Discussionmentioning

confidence: 99%

“…Binding of P-selectin to its main counter-receptor on monocytes, P-selectin glycoprotein ligand-1 (PSGL-1), leads to monocyte activation marked by the conformational activation of the ␤-2 integrin, MAC-1, 9 the synthesis and release of various cytokines, 10 chemokines, 11 and of reactive oxygen species. 12 Importantly, binding of P-selectin to PSGL-1 on monocytes also induces the expression of tissue factor (TF), 2 the main initiator of coagulation in vivo.…”

Section: See Page 877mentioning

confidence: 99%

Effect of P-Selectin on Phosphatidylserine Exposure and Surface-Dependent Thrombin Generation on Monocytes

Conde

Nabi

Tonda

et al. 2005

ATVB

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Objective-Stimulation of monocytes with P-selectin induces the synthesis of an array of mediators of inflammation, as well as the expression of tissue factor (TF), the main initiator of coagulation. Because the membrane-bound reactions of coagulation are profoundly influenced by the presence of phosphatidylserine on the membranes of cells, factors that increase its expression may have an impact on coagulation. Methods and Results-Using flow cytometry, we studied the effect of P-selectin on phosphatidylserine expression in blood monocytes and in the monocytic cells, THP-1. Soluble P-selectin at biologically relevant concentrations (0.31 to 2.5 g/mL) induced a time-dependent increase in phosphatidylserine expression, an effect that could be inhibited with an anti-PSGL-1 blocking antibody, and by genistein, a tyrosine kinase inhibitor. Binding of activated platelets to THP-1 cells also resulted in a significant increase in phosphatidylserine expression that was dependent on PSGL-1. Consistent with the role of phosphatidylserine on surface-dependent reactions of coagulation, treatment of monocytic cells with soluble P-selectin led to increased thrombin generation. We excluded P-selectin induced apoptosis of monocyte as a mechanism for the increased phosphatidylserine exposure. Conclusion-In summary, we show that P-selectin, either soluble or in its membrane-bound form, induces phosphatidylserine exposure in monocytes through a mechanism dependent on PSGL-

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Density‐dependent induction of TNF‐α release from human monocytes by immobilized P‐selectin

Cited by 36 publications

References 27 publications

Cytokine Secretion from Human Monocytes Potentiated by P-Selectin-Mediated Cell Adhesion

Cytokine Secretion from Human Monocytes Potentiated by P-Selectin-Mediated Cell Adhesion

Mechanism of transfusion-related acute lung injury induced by HLA class II antibodies

Effect of P-Selectin on Phosphatidylserine Exposure and Surface-Dependent Thrombin Generation on Monocytes

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