Modulation by cytokines of leukocyte-endothelial cell interactions. Implications for thrombosis

Beretz, Alain; Klein-Soyer, C; Archipoff, G; Camilla, Christophe; Brisson, Christine; Freyssinet, Jean‐Marie; Cazenave, Jean‐Pierre

doi:10.3233/bir-1990-273-423

Cited by 12 publications

(6 citation statements)

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“…Cytokines/chemokines secreted from the endothelium are mediators of complex interactions between endothelial cells and blood cells including immunocompetent leukocytes . They also have an autocrine function and regulate the interaction of endothelial cells with cellular microenvironments such as neighboring cells, extracellular matrix, and interstitial fluids. , Thus, endothelial secretion of cytokines/chemokines could affect major vascular events involved in immunity, inflammation, hemostasis, and angiogenesis .…”

Section: Resultsmentioning

confidence: 99%

Combined Effects of Substrate Topography and Stiffness on Endothelial Cytokine and Chemokine Secretion

Jeon¹,

Tsui

Jang³

et al. 2015

ACS Appl. Mater. Interfaces

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Endothelial physiology is regulated not only by humoral factors but also by mechanical factors such as fluid shear stress and the underlying cellular matrix microenvironment. The purpose of the present study was to examine the effects of matrix topographical cues on the endothelial secretion of cytokines/chemokines in vitro. Human endothelial cells were cultured on nanopatterned polymeric substrates with different ratios of ridge to groove widths (1:1, 1:2, and 1:5) and with different stiffnesses (6.7 MPa and 2.5 GPa) in the presence and absence of 1.0 ng/mL TNF-α. The levels of cytokines/chemokines secreted into the conditioned media were analyzed with a multiplexed bead-based sandwich immunoassay. Of the nano-patterns tested, the 1:1 and 1:2 type-patterns were found to induce the greatest degree of endothelial cell elongation and directional alignment. The 1:2 type nanopatterns lowered the secretion of inflammatory cytokines such as IL-1β, IL-3 and MCP-1, compared to unpatterned substrates. Additionally, of the two polymers tested, it was found that the stiffer substrate resulted in significant decreases in the secretion of IL-3 and MCP-1. These results suggest that substrates with specific extracellular nanotopographical cues or stiffnesses may provide anti-atherogenic effects like those seen with laminar shear stresses by suppressing the endothelial secretion of cytokines and chemokines involved in vascular inflammation and remodeling.

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Section: Resultsmentioning

confidence: 99%

Combined Effects of Substrate Topography and Stiffness on Endothelial Cytokine and Chemokine Secretion

Jeon¹,

Tsui

Jang³

et al. 2015

ACS Appl. Mater. Interfaces

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“…In the inflammation-related cytokine cascade (13), TNF-␣ and IL-1␤ are initially released from the site of inflammation and are then referred to as proinflammatory cytokines in the early stage; then, IL-6 (27) and IL-10 (25) are released, having an anti-inflammatory effect by inhibiting the production of TNF-␣, IL-1␤, and chemokine IL-8. Numerous studies have shown that some cytokines such as IL-1␤ promote platelet reactivity and the capacity of activated platelets to adhere to leukocytes by modulating the expression of adhesion molecules on platelets and leukocytes (5,22,31). According to previous investigations, vigorous, resistive, or eccentric exercises increased the amount of IL-1␤ released from exercising muscles, but this cytokine remained unchanged in response to aerobic and submaximal exercise (8,14,23,29).…”

Section: Discussionmentioning

confidence: 98%

“…The accumulation and activation of eosinophils and neutrophil and their subsequent interaction with platelets are critical in determining the severity of inflammation and thrombosis (3,7,32). Some inflammation-related cytokines have been observed to enhance platelet reactivity and subsequently increase the capacity of platelets to adhere to leukocytes (5,22,31). Although previous studies demonstrated that severe exercise enhanced neutrophil-and eosinophil-platelet aggregation (33) and inflammatory cytokine releases (23), the effects of chronic IH on the thromboinflammatory responses to this exercise remain unclear.…”

Section: Wang J-s Lin H-y Cheng M-l Wong M-kmentioning

confidence: 99%

Chronic intermittent hypoxia modulates eosinophil- and neutrophil-platelet aggregation and inflammatory cytokine secretion caused by strenuous exercise in men

Lin¹,

Cheng²,

Wong³

2007

Journal of Applied Physiology

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Although acclimatization to intermittent hypoxia (IH) improves exercise performance by increasing oxygen delivery and utilization, the effects of chronic IH on platelet-leukocyte interaction and inflammation-related cytokine secretion caused by strenuous exercise remain unclear. This investigation elucidates how two intensities of IH influence eosinophil- and neutrophil-platelet aggregation (EPA and NPA) as well as pro- and anti-inflammatory cytokines mediated by strenuous exercise. Twenty healthy sedentary men were randomly divided into severe (SIH) and moderate (MIH) IH groups; groups were exposed to 12% O2 (SIH) and 15% O2 (MIH) for 1 h/day, respectively, for 5 days/wk for 8 wk in a normobaric hypoxia chamber. Before IH intervention, 1) exercise up to maximal oxygen consumption promoted shear stress-, LPS-, and N-formyl-methionyl-leucyl-phenylalanine-induced EPA, increased IL-1beta and malondialdehyde levels, and decreased total antioxidant levels in plasma and 2) exposure to 12% O2, but not to 15% O2 for 1 h, enhanced LPS-induced EPA and reduced plasma total antioxidant levels. After IH for 8 wk, hypoxia- and exercise-promoted EPA, IL-1beta, or malondialdehyde levels were suppressed in both MIH and SIH groups, and plasma IL-6 and IL-10 levels in the SIH group were increased. However, the NPA induced by the shear force and chemical agonists was not changed under the two IH regimens. Therefore, both MIH and SIH regimens ameliorate eosinophil- and platelet-related thrombosis, proinflammatory IL-1beta secretion, and lipid peroxidation enhanced by strenuous exercise. Furthermore, SIH simultaneously increases circulatory anti-inflammatory IL-6 and IL-10 concentrations. These findings can help to develop effective IH regimens that improve aerobic fitness and minimize risk of thromboinflammation.

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“…Indeed, soluble thrombomodulin (sTM) is increased where there is endothelial cell membrane injury due to neutrophil‐derived proteolytic enzymes and inflammatory cytokines such as TNF‐α. However, IL‐1 and TNF‐α, both inflammatory cytokines, have been shown to downregulate TM expression by the endothelial cell [35,36]. As IL‐1 and TNF‐α levels are raised in HF, a more prothrombotic endothelial surface would therefore result.…”

Section: Endothelial Dysfunction Inflammation and Thrombogenesismentioning

confidence: 99%

Viewpoint: The prothrombotic state in heart failure: A maladaptive inflammatory response?

Chong

Lip

2007

European J of Heart Fail

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Patients with heart failure (HF) are at an increased risk of stroke, sudden death and venous thromboembolism, which are all linked to thrombus formation (thrombogenesis). The present 'viewpoint' article will discuss how the prothrombotic state in HF may be perpetuated by a chronic inflammatory state that is maladaptive. Indeed, there is considerable evidence that thrombogenesis and endothelial (dys)function can be intimately linked to inflammation in HF.

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Modulation by cytokines of leukocyte-endothelial cell interactions. Implications for thrombosis

Cited by 12 publications

References 0 publications

Combined Effects of Substrate Topography and Stiffness on Endothelial Cytokine and Chemokine Secretion

Combined Effects of Substrate Topography and Stiffness on Endothelial Cytokine and Chemokine Secretion

Chronic intermittent hypoxia modulates eosinophil- and neutrophil-platelet aggregation and inflammatory cytokine secretion caused by strenuous exercise in men

Viewpoint: The prothrombotic state in heart failure: A maladaptive inflammatory response?

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