Modulation of platelet and monocyte function by the chemokine fractalkine (<scp>CX</scp><sub>3</sub><scp>CL</scp>1) in cardiovascular disease

Flierl, Ulrike; Bauersachs, Johann; Schäfer, Andreas

doi:10.1111/eci.12443

Cited by 44 publications

(45 citation statements)

References 79 publications

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“…RA patients have a high risk of developing atherosclerosis and consequently cardiovascular disease; 30–50% of RA patients die for these causes. This is partly because these patients have different endothelial alterations, such as persistent activation, prothrombotic properties, and a reduction on vasodilator response [49–51]. Bergholm et al in 2002 were the first to identify endothelial dysfunction in RA patients.…”

Section: Endothelial Alterations In Sle and Ra: Potential Contribumentioning

confidence: 99%

Endothelial Alterations in Systemic Lupus Erythematosus and Rheumatoid Arthritis: Potential Effect of Monocyte Interaction

Atehortúa

Rojas

Vásquez

et al. 2017

Mediators of Inflammation

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Patients with systemic autoimmune diseases such as rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE) are prone to develop atherosclerosis and cardiovascular diseases five times more often than the general population; this increase in frequency could be partially explained by an increase in the macrovasculature endothelial damage. In these autoimmune diseases, a microvascular endothelial injury has also been reported in different organs and tissues, especially in sites where ultrafiltration processes occur. Different components that are characteristic to the immunopathology of RA and SLE could be involved in the endothelial cell activation, permeability increase, functional alteration, and vascular injury. Circulating immune complexes (IC) detected in SLE and RA have been proposed to participate in the endothelial injury. In the vascular environment, IC can generate different responses that could be mediated by monocytes, because these cells have patrolling and monitoring functions on the endothelium. However, with certain stimuli such as TLR ligands, the monocytes are retained in the lumen, releasing proinflammatory mediators that participate in the endothelial damage. This paper aims to review some aspects about the endothelial activation and dysfunction in the context of SLE and RA, as well as the potential role that monocytes apparently play in this process.

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Section: Endothelial Alterations In Sle and Ra: Potential Contribumentioning

confidence: 99%

Endothelial Alterations in Systemic Lupus Erythematosus and Rheumatoid Arthritis: Potential Effect of Monocyte Interaction

Atehortúa

Rojas

Vásquez

et al. 2017

Mediators of Inflammation

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“…In addition, experiment evidences have described the active involvement of CX3CL1/CX3CR1 in many other diseases, such as atherosclerotic, allergic asthma and rhinitis, renal diseases, rheumatoid arthritis (RA), Sjögren's syndrome (SS), systemic lupus erythematosus (SLE), scleroderma, colorectal cancer, and breast cancer [ 117 – 123 ]. For example, a genetically defined less active CX3CL1/CX3CR1 pathway is associated with a reduced risk of atherosclerotic disease in humans and the blockade of the CX3CL1/CX3CR1 pathway ameliorates the severity of atherosclerosis [ 124 , 125 ].…”

Section: Discussionmentioning

confidence: 99%

CX3CL1/CX3CR1 in Alzheimer’s Disease: A Target for Neuroprotection

Chen

Zhao

Guo

et al. 2016

BioMed Research International

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CX3C chemokine ligand 1 (CX3CL1) is an intriguing chemokine belonging to the CX3C family. CX3CL1 is secreted by neurons and plays an important role in modulating glial activation in the central nervous system after binding to its sole receptor CX3CR1 which mainly is expressed on microglia. Emerging data highlights the beneficial potential of CX3CL1-CX3CR1 in the pathogenesis of Alzheimer's disease (AD), a common progressive neurodegenerative disease, and in the progression of which neuroinflammation plays a vital role. Even so, the importance of CX3CL1/CX3CR1 in AD is still controversial and needs further clarification. In this review, we make an attempt to present a concise map of CX3CL1-CX3CR1 associated with AD to find biomarkers for early diagnosis or therapeutic interventions.

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“…Platelet-leukocyte conjugates were chosen because they are known to be more sensitive and longer-lived markers of in vivo platelet activation than surface P-selectin expression. 32,34,35 Secondary outcomes were the transcerebral gradients of activated monocytes and neutrophils. The transcerebral gradient was determined by subtracting the arterial value from the corresponding jugular venous value.…”

Section: Methodsmentioning

confidence: 99%

Effect of intravenous lidocaine on the transcerebral inflammatory response during cardiac surgery: a randomized-controlled trial

Klinger

Cooter

Berger

et al. 2016

Can J Anesth/J Can Anesth

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Purpose Postoperative cognitive dysfunction (POCD) occurs frequently after cardiac surgery. The pathophysiology of POCD remains elusive, but previous work showed that intravenous lidocaine may be protective against POCD, possibly by modulating cerebral inflammation. We hypothesized that intravenous lidocaine would attenuate the cerebral inflammatory response to cardiopulmonary bypass (CPB) by reducing the transcerebral activation gradients of platelets, leukocytes, and/or platelet-leukocyte conjugates. Methods We studied 202 patients undergoing cardiac surgery with CPB in this prospective randomized doubleblinded placebo-controlled trial. Subjects were randomized to receive either intravenous lidocaine (bolus ? 48-hr infusion) or placebo (identical infusion volume and duration). Paired jugular venous and radial arterial blood samples were drawn at several time points and analyzed by fluorescence-activated cell sorting to identify activated platelets and plateletleukocyte conjugates. Transcerebral activation gradients were calculated by subtracting arterial values from venous values and were compared between groups using repeated measures regression models with covariate adjustment for age, sex, surgery type, and CPB duration. Results Beginning after aortic cross-clamp release and peaking ten minutes after the termination of CPB, the mean (SD) transcerebral activation gradient of platelet-monocyte conjugates decreased in lidocaine-treated vs placebo-treated patients [-1.84 (11.47) mean linear fluorescence intensity (MLFI) vs 1.46 (13.88) MLFI, respectively; mean difference, -4.08 MLFI; 95% confidence interval, -7.86 to -0.29; P = 0.03). No difference was seen at any time point for activated platelets or for platelet-neutrophil conjugates. Conclusion While lidocaine did not affect the systemic or transcerebral activation of platelets or leukocytes, we did observe a reduction in the transcerebral activation of platelet-monocyte conjugates after aortic cross-clamp release. This may be a manifestation of reduced cerebral inflammation during cardiopulmonary bypass in response to treatment with lidocaine. This trial was registered at ClinicalTrials.gov (NCT00938964). RésuméObjectif Le dysfonctionnement cognitif postopératoire (DCPO) constitue une complication fréquente après une A list of all members of the Neurologic Outcome Research Group is given in the Appendix.

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Modulation of platelet and monocyte function by the chemokine fractalkine (CX₃CL1) in cardiovascular disease

Cited by 44 publications

References 79 publications

Endothelial Alterations in Systemic Lupus Erythematosus and Rheumatoid Arthritis: Potential Effect of Monocyte Interaction

Endothelial Alterations in Systemic Lupus Erythematosus and Rheumatoid Arthritis: Potential Effect of Monocyte Interaction

CX3CL1/CX3CR1 in Alzheimer’s Disease: A Target for Neuroprotection

Effect of intravenous lidocaine on the transcerebral inflammatory response during cardiac surgery: a randomized-controlled trial

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Modulation of platelet and monocyte function by the chemokine fractalkine (CX3CL1) in cardiovascular disease

Cited by 44 publications

References 79 publications

Endothelial Alterations in Systemic Lupus Erythematosus and Rheumatoid Arthritis: Potential Effect of Monocyte Interaction

Endothelial Alterations in Systemic Lupus Erythematosus and Rheumatoid Arthritis: Potential Effect of Monocyte Interaction

CX3CL1/CX3CR1 in Alzheimer’s Disease: A Target for Neuroprotection

Effect of intravenous lidocaine on the transcerebral inflammatory response during cardiac surgery: a randomized-controlled trial

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Modulation of platelet and monocyte function by the chemokine fractalkine (CX₃CL1) in cardiovascular disease