A wide variety of inflammatory mediators, mainly cytokines and chemokines, are induced during SARS CoV-2 infection. Among these proinflammatory mediators, chemokines tend to play a pivotal role in virus-mediated immunopathology. The C-C chemokine ligand 2 (CCL2), also known as monocyte chemoattractant protein-1 (MCP-1) is a potent proinflammatory cytokine and strong chemoattractant of monocytes, macrophages and CD4+ T cells bearing C-C chemokine receptor type-2 (CCR2). Besides controlling immune cell trafficking, CCL2 is also involved in multiple pathophysiological processes including systemic hyperinflammation associated cytokine release syndrome (CRS), organ fibrosis and blood coagulation. These pathological features are commonly manifested in severe and fatal cases of COVID-19. Given the crucial role of CCL2 in COVID-19 pathogenesis, the CCL2:CCR2 axis may constitute a potential therapeutic target to control virus-induced hyperinflammation and multi-organ dysfunction. Herein we describe recent advances on elucidating the role of CCL2 in COVID-19 pathogenesis, prognosis, and a potential target of anti-inflammatory interventions.

Download full-text PDF

Source
http://dx.doi.org/10.1002/rmv.2578DOI Listing

Publication Analysis

Top Keywords

ccl2 covid-19
12
covid-19 pathogenesis
12
target anti-inflammatory
8
c-c chemokine
8
role ccl2
8
ccl2
5
virus-induced host
4
host chemokine
4
chemokine ccl2
4
covid-19
4

Similar Publications

Basic Science and Pathogenesis.

Alzheimers Dement

December 2024

Department of Neurosurgery, Clinical Neuroscience Research Center, Tulane University School of Medicine, New Orleans, LA, USA.

Background: SARS-CoV-2 causes a variety of neurological sequelae in COVID-19 survivors, including fatigue and cognitive dysfunction. Endothelial dysfunction is the unifying and central mechanism of COVID-19 illness and a major risk factor for vascular dementia (VaD). Endothelial dysfunction stems, in part, from an imbalance between nitric oxide (NO) generated by the endothelial nitric oxide synthase (eNOS) and reactive oxidant species produced by uncoupled-eNOS.

View Article and Find Full Text PDF

Objective: are clinically relevant for severity prediction and treatment of COVID-19 caused by SARS-CoV-2. We aimed to demonstrate the potential cytokines for severity prediction in the five days after symptom onset and describe the importance of serum cytokine levels for patients with different disease severity.

Materials And Methods: Hospitalized COVID-19 patients and healthy control participants were recruited, and serial sera were collected from COVID-19 patients.

View Article and Find Full Text PDF

SARS-CoV-2 ORF8 drives osteoclastogenesis in preexisting immune-mediated inflammatory diseases.

JCI Insight

December 2024

Infection Biology Program, Global Center for Pathogen Research and Human Health, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio, USA.

Patients with immune-mediated inflammatory diseases (IMIDs) like rheumatoid arthritis (RA) are at higher risk for severe COVID-19 and long-term complications in bone health. Emerging clinical evidence demonstrated that SARS-CoV-2 infection reduces bone turnover and promotes bone loss, but the mechanism underlying worsened bone health remains elusive. This study sought to identify specific immune mediators that exacerbated preexisting IMIDs after SARS-CoV-2 exposure.

View Article and Find Full Text PDF

Growing evidence suggests the neurobiological mechanism upholding post-COVID-19 depression mainly relates to immune response and subsequent unresolved low-grade inflammation. Herein we exploit a broad panel of cytokines serum levels measured in COVID-19 survivors at one- and three-month since infection to predict post-COVID-19 depression. 87 COVID survivors were screened for depressive symptomatology at one- and three-month after discharge through the Beck Depression Inventory (BDI-13) and the Zung Self-Rating Depression Scale (ZSDS) at San Raffaele Hospital.

View Article and Find Full Text PDF

Predicting survival in patients with SARS-CoV-2 based on cytokines and soluble immune checkpoint regulators.

Front Cell Infect Microbiol

December 2024

Department of Laboratory Medicine, Hallym University College of Medicine, Kangnam Sacred Heart Hospital, Seoul, Republic of Korea.

Background: Coronavirus disease 2019 (COVID-19) has been widespread for over four years and has progressed to an endemic stage. Accordingly, the evaluation of host immunity in infected patients and the development of markers for prognostic prediction in the early stages have been emphasized. Soluble immune checkpoints (sICs), which regulate T cell activity, have been reported as promising biomarkers of viral infections.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!