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Review
. 2024 Sep;34(5):e2578.
doi: 10.1002/rmv.2578.

Virus-Induced Host Chemokine CCL2 in COVID-19 Pathogenesis: Potential Prognostic Marker and Target of Anti-Inflammatory Strategy

Abdul Wahid Ansari  1 , Fareed Ahmad  1 , Majid Ali Alam  1 , Thesni Raheed  1 , Ahmed Zaqout  2   3 , Muna Al-Maslamani  2   3 , Aamir Ahmad  1 , Joerg Buddenkotte  1   4 , Abdullatif Al-Khal  2   3 , Martin Steinhoff  1   4   5   6   7   8
Affiliations
Review

Virus-Induced Host Chemokine CCL2 in COVID-19 Pathogenesis: Potential Prognostic Marker and Target of Anti-Inflammatory Strategy

Abdul Wahid Ansari et al. Rev Med Virol. 2024 Sep.

Abstract

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.

Keywords: ARDS; CCL2; COVID‐19; cytokine release syndrome; immunopathogenesis; multi‐organ dysfunction.

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