Circulating Leukocyte as an Inflammatory Biomarker: Association with Fibrinogen and Neuronal Damage in Acute Ischemic Stroke

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Abstract

Background and Purpose

Leukocytes and fibrinogen are inflammatory markers involved in circulating and central inflammatory response after ischemic stroke. However, the interaction between circulating leukocytes and serum fibrinogen and neuronal injury in acute ischemic stroke (AIS) patients is still unclear. The present study aimed to investigate the association between circulating leukocyte and serum fibrinogen and neuronal injury respectively in AIS.

Methods

A cross-section study with 431 hospitalized AIS patients from department of neurology was performed. Circulating leukocytes and fibrinogen were measured, and neuron-specific enolase (NSE) was detected to evaluate central neuronal damage. A propensity score matching method was used to minimize the effects of confounding factors. The relationship between leukocytes and NSE and fibrinogen was analyzed by linear curve fitting analysis and multiple logistic regression models respectively.

Results

The mean levels of NSE, leukocyte, and fibrinogen were significantly higher in the matched AIS group (n=89) than those of in the healthy control group (n=89) (all p<0.05). Both serum NSE and fibrinogen were increased with the increasing of leukocyte in AIS patients (both p<0.05). Smoothed plots suggested that there are linear relationships between leukocyte and NSE and fibrinogen respectively. Multiple logistic regression analysis showed the OR (95%) for the relationship between leukocyte and high NSE were 1.13 (1.01–1.26, p=0.031) and 1.13 (1.00–1.28, p=0.048), and between leukocyte and high fibrinogen were 1.40 (1.22–1.61, p<0.001) and 1.35 (1.15–1.58, p<0.001) in all AIS patients before and after adjusting for potential confounders.

Conclusion

Our study suggests that elevated circulating leukocyte was associated with high fibrinogen and neuronal injury in AIS. Therefore, there may be potential targets among circulating leukocyte, fibrinogen and NSE that should be intervened to reduce inflammatory reaction after ischemic stroke.

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Most cited references 45

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Global brain inflammation in stroke

Kaibin Shi, De-Cai Tian, Zhi-Guo Li … (2019)

Stroke, including acute ischaemic stroke and intracerebral haemorrhage, results in neuronal cell death and the release of factors such as damage-associated molecular patterns (DAMPs) that elicit localised inflammation in the injured brain region. Such focal brain inflammation aggravates secondary brain injury by exacerbating blood-brain barrier damage, microvascular failure, brain oedema, oxidative stress, and by directly inducing neuronal cell death. In addition to inflammation localised to the injured brain region, a growing body of evidence suggests that inflammatory responses after a stroke occur and persist throughout the entire brain. Global brain inflammation might continuously shape the evolving pathology after a stroke and affect the patients' long-term neurological outcome. Future efforts towards understanding the mechanisms governing the emergence of so-called global brain inflammation would facilitate modulation of this inflammation as a potential therapeutic strategy for stroke.

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Inflammatory mechanisms in ischemic stroke: role of inflammatory cells.

Rong Jin, Guojun Yang, Guohong Li (2010)

Inflammation plays an important role in the pathogenesis of ischemic stroke and other forms of ischemic brain injury. Experimentally and clinically, the brain responds to ischemic injury with an acute and prolonged inflammatory process, characterized by rapid activation of resident cells (mainly microglia), production of proinflammatory mediators, and infiltration of various types of inflammatory cells (including neutrophils, different subtypes of T cells, monocyte/macrophages, and other cells) into the ischemic brain tissue. These cellular events collaboratively contribute to ischemic brain injury. Despite intense investigation, there are still numerous controversies concerning the time course of the recruitment of inflammatory cells in the brain and their pathogenic roles in ischemic brain injury. In this review, we provide an overview of the time-dependent recruitment of different inflammatory cells following focal cerebral I/R. We discuss how these cells contribute to ischemic brain injury and highlight certain recent findings and currently unanswered questions about inflammatory cells in the pathophysiology of ischemic stroke.

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Interplay between inflammation and thrombosis in cardiovascular pathology

Konstantin Stark, Steffen Massberg (2021)

Thrombosis is the most feared complication of cardiovascular diseases and a main cause of death worldwide, making it a major health-care challenge. Platelets and the coagulation cascade are effectively targeted by antithrombotic approaches, which carry an inherent risk of bleeding. Moreover, antithrombotics cannot completely prevent thrombotic events, implicating a therapeutic gap due to a third, not yet adequately addressed mechanism, namely inflammation. In this Review, we discuss how the synergy between inflammation and thrombosis drives thrombotic diseases. We focus on the huge potential of anti-inflammatory strategies to target cardiovascular pathologies. Findings in the past decade have uncovered a sophisticated connection between innate immunity, platelet activation and coagulation, termed immunothrombosis. Immunothrombosis is an important host defence mechanism to limit systemic spreading of pathogens through the bloodstream. However, the aberrant activation of immunothrombosis in cardiovascular diseases causes myocardial infarction, stroke and venous thromboembolism. The clinical relevance of aberrant immunothrombosis, referred to as thromboinflammation, is supported by the increased risk of cardiovascular events in patients with inflammatory diseases but also during infections, including in COVID-19. Clinical trials in the past 4 years have confirmed the anti-ischaemic effects of anti-inflammatory strategies, backing the concept of a prothrombotic function of inflammation. Targeting inflammation to prevent thrombosis leaves haemostasis mainly unaffected, circumventing the risk of bleeding associated with current approaches. Considering the growing number of anti-inflammatory therapies, it is crucial to appreciate their potential in covering therapeutic gaps in cardiovascular diseases. In this Review, Stark and Massberg discuss how the interplay between innate immunity, platelet activation and coagulation, known as immunothrombosis, functions as a host defence mechanism to limit pathogen spreading, yet its aberrant activation, termed thromboinflammation, results in thrombotic complications, highlighting the therapeutic potential of anti-inflammatory strategies in cardiovascular pathologies. Inflammation and thrombosis are tightly connected processes that contribute to the containment of pathogen spreading in a host defence effector mechanism termed immunothrombosis. The dysregulated and excessive activation of immunothrombosis results in thromboinflammation, causing tissue ischaemia by microvascular and macrovascular thrombosis. The main factor in immunothrombosis and thromboinflammation is a vicious circle of platelet and innate immune cell activation, unleashing the complement system and coagulation cascade. Inflammatory conditions such as infection, chronic autoimmune diseases and clonal haematopoiesis of indeterminate potential are associated with an increased risk of thrombotic events, providing clinical evidence for the partnership between inflammation and thrombosis. Pulmonary immunothrombosis is a prominent feature of severe COVID-19, aggravating respiratory failure and correlating with a systemic prothrombotic phenotype. The inflammatory component of thrombosis is a therapeutic gap and a promising target for the prevention and treatment of cardiovascular diseases such as myocardial infarction, stroke and venous thromboembolism.

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Author and article information

Journal

Journal ID (nlm-ta): J Inflamm Res

Journal ID (iso-abbrev): J Inflamm Res

Journal ID (publisher-id): jir

Title: Journal of Inflammation Research

Publisher: Dove

ISSN (Electronic): 1178-7031

Publication date (Electronic): 21 March 2023

Publication date Collection: 2023

Volume: 16

Pages: 1213-1226

Affiliations

[1 ]Department of Neurology, Ren Ji Hospital, Shanghai Jiao Tong University School of Medicine , Shanghai, 200127, People’s Republic of China

[2 ]Department of Neurology, Baoshan Branch, Ren Ji Hospital, Shanghai Jiao Tong University School of Medicine , Shanghai, 200444, People’s Republic of China

Author notes

Correspondence: Yang-Tai Guan, Department of Neurology, Ren Ji Hospital, Shanghai Jiao Tong University School of Medicine , No. 160, Pujian Road, Shanghai, 200127, People’s Republic of China, Tel +86-13386271865, Fax +86-21-68383482, Email guanyangtai@renji.com

De-Sheng Zhu, Department of Neurology, Ren Ji Hospital, Shanghai Jiao Tong University School of Medicine , No. 160, Pujian Road, Shanghai, 200127, People’s Republic of China, Tel +86-13564719779, Email deshengzhu2008@sina.com

Author information

Lu Han http://orcid.org/0000-0002-9912-1384

De-Sheng Zhu http://orcid.org/0000-0003-2454-2173

Article

Publisher ID: 399021

DOI: 10.2147/JIR.S399021

PMC ID: 10039626

PubMed ID: 36974204

SO-VID: 27742adf-7417-4cf2-9753-07fcf609b235

License:

This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms ( https://www.dovepress.com/terms.php).

History

Date received : 30 November 2022

Date accepted : 14 March 2023

Page count

Figures: 5, Tables: 4, References: 45, Pages: 14

Funding

Funded by: Shanghai Cooperative Innovation Center for Translational Medicine;

Funded by: Shanghai Shenkang hospital development center clinical three-year action plan;

Funded by: Key projects of basic research of Shanghai Municipal Science and Technology Commission;

This work was supported by the Shanghai Cooperative Innovation Center for Translational Medicine (No. TM201706), the Shanghai Shenkang hospital development center clinical three-year action plan (No. SHDC2020CR2024B), and the Key projects of basic research of Shanghai Municipal Science and Technology Commission (No. 20JC1412000).

Circulating Leukocyte as an Inflammatory Biomarker: Association with Fibrinogen and Neuronal Damage in Acute Ischemic Stroke

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Abstract

Background and Purpose

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Gamma Delta T cells

Most cited references 45

Global brain inflammation in stroke

Inflammatory mechanisms in ischemic stroke: role of inflammatory cells.

Interplay between inflammation and thrombosis in cardiovascular pathology

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Journal

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