As of the end of 2020, coronavirus disease 2019 (COVID-19) remains a global healthcare challenge with alarming death tolls. In the absence of targeted therapies, supportive care continues to be the mainstay of treatment. The hallmark of severe COVID-19 is a thromboinflammatory storm driven by innate immune responses. This manifests clinically as acute respiratory distress syndrome, and in some patients, widespread thrombotic microangiopathy. Neutrophils and complement are key players in the innate immune system, and their role in perpetuating fatal severe COVID-19 continues to receive increasing attention. Here, we review the interplay between neutrophils, neutrophil extracellular traps, and complement in COVID-19 immunopathology, and highlight potential therapeutic strategies to combat these pathways.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7831864 | PMC |
| http://dx.doi.org/10.1016/j.berh.2021.101661 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Neutrophil Elastase as A Potential Target in Ischemia-Reperfusion Injury.
Curr Vasc Pharmacol
January 2025
Department of Pharmacy, Peking Union Medical College Hospital, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing, China.
Neutrophil elastase (NE), a major protease in neutrophils, is important in promoting inflammation and multiple pathological processes. While NE is released abundantly in ischemiareperfusion (I/R) injury, the intricate relationship between NE and I/R injury remains unclear. We examine several aspects of how NE is involved in I/R injury.
View Article and Find Full Text PDFPPARα suppresses growth of hepatocellular carcinoma in a high-fat diet context by reducing neutrophil extracellular trap release.
JHEP Rep
January 2025
Department of Hepatobiliary Surgery and Fujian Institute of Hepatobiliary Surgery, Fujian Medical University Union Hospital, Fuzhou, China.
Background & Aims: The role of infiltrating neutrophils in hepatocellular carcinoma (HCC) is modulated by cellular metabolism, specifically lipid homeostasis. Throughout the progression of HCC, alterations in lipid metabolism are intricately linked with regulation of neutrophil function and the release of neutrophil extracellular traps (NETs). However, how much the protumor effect of a high-fat diet (HFD) depends on NETs and the potential interplay between NETs and other leukocytes in HCC remains uncertain.
View Article and Find Full Text PDFInterplay between circulating von Willebrand factor and neutrophils: implications for inflammation, neutrophil function, and von Willebrand factor clearance.
Haematologica
January 2025
Institute of Experimental Haematology and Transfusion Medicine, University Hospital Bonn, Bonn.
Von Willebrand factor (VWF) plays a critical role in hemostasis, and emerging evidence suggests its involvement in inflammation. Our study aimed to investigate the interaction between circulating plasma VWF and neutrophils (polymorphonuclear cells, PMNs), elucidate the fate of VWF after binding, and explore its impact on neutrophil behavior. Neutrophils were isolated from the whole blood of healthy volunteers, and their interaction with plasma VWF was examined ex vivo.
View Article and Find Full Text PDFMacrophages and Pulmonary Fibrosis.
Curr Mol Med
January 2025
Department of Respiratory and Critical Care Medicine, Binzhou Medical University Hospital, Binzhou Medical University, Binzhou 256603, China.
Most chronic respiratory diseases often lead to the clinical manifestation of pulmonary fibrosis. Inflammation and immune disorders are widely recognized as primary contributors to the onset of pulmonary fibrosis. Given that macrophages are predominantly responsible for inflammation and immune disorders, in this review, we first focused on the role of different subpopulations of macrophages in the lung and discussed the crosstalk between macrophages and other immune cells, such as neutrophils, regulatory T cells, NKT cells, and B lymphocytes during pulmonary fibrogenesis.
View Article and Find Full Text PDFDual ASXL1 and CSF3R mutations drive myeloid biased stem cell expansion and enhance neutrophil differentiation.
Blood Adv
January 2025
Oregon Health & Science University, Portland, Oregon, United States.
Mutations in the epigenetic regulator Additional Sex Combs-Like 1 (ASXL1) are frequently observed in chronic neutrophilic leukemia (CNL). CNL is a myeloproliferative neoplasm (MPN) driven by activating mutations in the Colony Stimulating Factor 3 Receptor (CSF3R), which cause excessive neutrophil production. Despite the high rates of co-occurrence, the interplay between ASXL1 and CSF3R mutations in hematopoiesis and leukemia remains poorly understood.
View Article and Find Full Text PDFWant 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!