Platelet-leukocyte crosstalk: Linking proinflammatory responses to procoagulant state

Ghasemzadeh, Mehran; Hosseini, Ehteramolsadat

doi:10.1016/j.thromres.2012.11.028

Cited by 131 publications

(108 citation statements)

References 106 publications

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“…It has been demonstrated that human neutrophils, other than interacting with nonimmune cell types such as platelets 39 and mesenchimal stem cells, 3 can establish, in vitro and in vivo, cross-talk with innate immune cells, such as DCs, monocytes, macrophages, and natural killer (NK) cells, as well as with adaptive immune cells, such as T and B cells, or related subpopulations [3][4][5][6] (summarized in Tables 1 and 2). As highlighted below, by establishing such bidirectional interactions, neutrophils receive signals modulating their survival and effector functions on the one hand, whereas they initiate, amplify, and/or suppress innate or adaptive immune effector responses on the other hand.…”

Section: Neutrophil-centered Cross-talkmentioning

confidence: 99%

Social networking of human neutrophils within the immune system

Scapini

Cassatella

2014

Blood

337

320

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It is now widely recognized that neutrophils are highly versatile and sophisticated cells that display de novo synthetic capacity and may greatly extend their lifespan. In addition, concepts such as “neutrophil heterogeneity” and “neutrophil plasticity” have started to emerge, implying that, under pathological conditions, neutrophils may differentiate into discrete subsets defined by distinct phenotypic and functional profiles. A number of studies have shown that neutrophils act as effectors in both innate and adaptive immunoregulatory networks. In fact, once recruited into inflamed tissues, neutrophils engage into complex bidirectional interactions with macrophages, natural killer, dendritic and mesenchymal stem cells, B and T lymphocytes, or platelets. As a result of this cross-talk, mediated either by contact-dependent mechanisms or cell-derived soluble factors, neutrophils and target cells reciprocally modulate their survival and activation status. Altogether, these novel aspects of neutrophil biology have shed new light not only on the potential complex roles that neutrophils play during inflammation and immune responses, but also in the pathogenesis of several inflammatory disorders including infection, autoimmunity, and cancer.

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Section: Neutrophil-centered Cross-talkmentioning

confidence: 99%

Social networking of human neutrophils within the immune system

Scapini

Cassatella

2014

Blood

337

320

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“…1 However, the details of the complex crosstalk between inflammation and hemostasis are far to be elucidated. [2][3][4][5][6][7][8] Some interesting animal models of inflammation-induced thrombosis exist, 9,10 but human models have not been yet proposed.…”

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confidence: 99%

Neutrophil Activation Promotes Fibrinogen Oxidation and Thrombus Formation in Behçet Disease

et al. 2016

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Background-Behçet disease (BD) is a systemic vasculitis with a broad range of organ involvement, characterized by a multisystemic, immune-inflammatory disorder involving vessels of all sizes and often complicated by thrombosis. Systemic redox imbalance and circulating neutrophil hyperactivation have been observed in BD patients and are thought to be responsible for impaired coagulation. We here focused on the pathogenetic mechanisms potentially linking immune cell activation and thrombosis, and specifically examined whether neutrophil activation can affect fibrinogen modifications and consequently elicit thrombosis. Methods and Results-Blood samples were collected from 98 consecutive BD patients attending our dedicated Center and from 70 age-and sex-matched healthy controls; in all patients fibrinogen function and structure, fibrin susceptibility to plasmin-lysis, plasma redox status, leukocyte oxidative stress markers, and possible reactive oxygen species sources were examined. Thrombin-catalyzed fibrin formation and fibrin susceptibility to plasmin-induced lysis were significantly impaired in BD patients (P<0.001). These findings were associated with increased plasma oxidative stress markers (P<0.001) and with a marked carbonylation of fibrinogen (P<0.001), whose secondary structure appeared deeply modified. Neutrophils displayed an enhanced NADPH oxidase activity and increased reactive oxygen species production (P<0.001), which significantly correlated with fibrinogen carbonylation level (r 2 =0.33, P<0.0001), residual β-band intensity (r 2 =0.07, P<0.01), and fibrinogen clotting ability (r 2 =0.073, P<0.01) Conclusions-In BD patients, altered fibrinogen structure and impaired fibrinogen function are associated with neutrophil activation and enhanced reactive oxygen species production whose primary source is represented by neutrophil NADPH oxidase. Becatti et al Role of Neutrophils in Thrombus Formation 303for the management of BD suggest that thrombosis should be treated with immunosuppression rather than anticoagulation, 17 as an inflammation-induced thrombosis. Recent studies have provided evidence that fibrinogen plays a multifaceted role in inflammatory responses and autoimmunity. 18,19 The ability of fibrinogen to participate in the inflammatory response depends on its specific interaction with integrins, the leukocyte cell surface adhesion receptors. M2 (CD11b/CD18, Mac-1) and X2 (CD11c/CD18, p150,95) are the main fibrinogen receptors and are expressed on neutrophils, monocytes, macrophages and several subsets of lymphocytes. 20 In BD, endothelial cell dysfunction, increased reactive oxygen species (ROS) production, 21 and neutrophil hyperfunction have been reported, 15 together with an impaired fibrinolysis. 22 In this study, to highlight the mechanisms of inflammation-induced thrombosis, we investigated fibrinogen modifications, fibrin susceptibility to plasmin-lysis, plasma redox status, leukocyte oxidative stress, and possible ROS sources in a population of BD patients. Moreover, we explored fib...

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“…Interestingly, cancer cells can recruit and activate various leukocytes (especially neutrophils and monocytes) by T cells, specific chemokines and prostaglandins [17][18][19][20]. Moreover, the activation of platelet stimulated by proinflammatory cytokines participates in neutrophil recruitment and promotes inflammatory response [21]. The inflammatory response to tumor may contribute to tumor growth, progression and metastasis through several mechanisms, including the up-regulation of inflammatory mediators and cytokine, aberrant activation of immune regulatory cytokines, suppression of apoptosis, and DNA damage [22].…”

Section: Introductionmentioning

confidence: 99%

“…In recent years, several indicators derived from the peripheral blood such as the neutrophil to lymphocyte ratio (NLR), derived neutrophil to lymphocyte ratio (dNLR), platelet to lymphocyte ratio (PLR) and lymphocyte to monocyte ratio (LMR) have been widely investigated as useful prognostic indicators in various kinds of cancers including gastric cancer, colorectal cancer, hepatocellular carcinoma, non-small cell lung cancer, breast cancer and pancreatic cancer [23][24][25][26][27]. However, only one or two inflammatory biomarkers have been evaluated for the prognosis of patients with gastric cancer according to previous reports [11,[17][18][19][20][21]. Moreover, the optimal cut-off values of the biomarkers from these studies were still inconsistent.…”

Section: Introductionmentioning

confidence: 99%

The Role of Baseline Inflammatory Response Biomarkers in Predictingthe Prognosis in No Metastatic Gastric Cancer Patients Treated with Preoperative Chemoradiation

Zaghloul¹,

Abbas²

2017

J Cancer Sci Ther

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Purpose: To evaluate the prognostic potential of inflammatory response biomarkers neutrophil to lymphocyte ratio (NLR), derived neutrophil to lymphocyte ratio (dNLR), platelet to lymphocyte ratio (PLR) and lymphocyte to monocyte ratio (LMR) in predicting the outcome of gastric cancer patients undergoing neoadjuvant chemoradiation prior to surgical resection. Methods:Patients with localized, gastric adenocarcinoma received two cycles of induction chemotherapy of fluorouracil, docetaxel, and cisplatin (TPF) followed by 45 Gy of radiation and concurrent fluorouracil plus docetaxel then surgery for non-metastatic patients. Baseline NLR, dNLR, PLR and LMR calculated from peripheral blood cell count taken at pre-operation were compared with clinicopathological parameters. The prognostic value of baseline NLR, dNLR, PLR and LMR for disease free survival (DFS) and overall survival (OS) were assessed using Log rank and Cox regression. Results:The final analysis included 80 patient who had resection after neoadjuvant chemoradiation. The receiver operating curve (ROC) cut off values of baseline NLR, dNLR, LMR and PLR in predicting outcome were 2.4, 1.7, 5.1 and 130 respectively. Elevated NLR, dNLR, PLR, LMR, age of patients (≥ 50 years), stage III, grade 3 tumors, R1 resection and partial response to preoperative chemoradiation course with >10% residual tumor were significantly associated with decreased OS, and DFS. Multivariate analysis revealed that elevated NLR and dNLR were independent factors for worse OS and DFS hazard ratio (HR) 2.04 (95% CI=2.41-8.24), 6.63 (95% CI, 1.61-10.32) and DSF with (HR) 1.84 (95% CI=3.27-7.36), 4.63 (95% CI=3.61-12.12) respectively. Conclusion:The baseline NLR, dNLR, LMR and PLR showed a significant association with different clinicopathological prognostic factors in gastric cancer patients receiving preoperative chemoradiation. Additionally, NLR, dNLR may be considered as potential independent prognostic indicators of clinical outcomes in this group of patients.

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Platelet-leukocyte crosstalk: Linking proinflammatory responses to procoagulant state

Cited by 131 publications

References 106 publications

Social networking of human neutrophils within the immune system

Social networking of human neutrophils within the immune system

Neutrophil Activation Promotes Fibrinogen Oxidation and Thrombus Formation in Behçet Disease

The Role of Baseline Inflammatory Response Biomarkers in Predictingthe Prognosis in No Metastatic Gastric Cancer Patients Treated with Preoperative Chemoradiation

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