ArticleProceedings of the National Academy of Sciences of the United States of America2019
BCL6 modulates tissue neutrophil survival and exacerbates pulmonary inflammation following influenza virus infection.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 73 citations in OpenAlex.
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- IFN-γ primes bone marrow neutrophils to acquire regulatory functions in severe viral respiratory infections.Science advances · 2024Article
- Tolerance to Haemophilus influenzae infection in human epithelial cells: Insights from a primary cell-based model.PLoS pathogens · 2024Article
- Generic model to unravel the deeper insights of viral infections: an empirical application of evolutionary graph coloring in computational network biology.BMC bioinformatics · 2024Article
- Exploring the pathogenesis and key genes associated of acute myocardial infarction complicated with Alzheimer's disease.Scientific reports · 2024Article
- Neutrophil-specific ORAI1 Calcium Channel Inhibition Reduces Pancreatitis-associated Acute Lung Injury.Function (Oxford, England) · 2024Article
- miR-346 regulates the development of ARDS by regulating the function of pulmonary microvascular endothelial cells.Non-coding RNA research · 2023Article
- Biologic Mechanisms of Macrophage Phenotypes Responding to Infection and the Novel Therapies to Moderate Inflammation.International journal of molecular sciences · 2023Review
- Immune cells and their related genes provide a new perspective on the common pathogenesis of ankylosing spondylitis and inflammatory bowel diseases.Frontiers in immunology · 2023Article
- Bcl6 drives stem-like memory macrophages differentiation to foster tumor progression.Cellular and molecular life sciences : CMLS · 2022Article
- Article
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- Mesenchymal Stem Cell-Derived Extracellular Vesicle-Shuttled microRNA-302d-3p Represses Inflammation and Cardiac Remodeling Following Acute Myocardial Infarction.Journal of cardiovascular translational research · 2022Article
- TFAM-Dependent Mitochondrial Metabolism Is Required for Alveolar Macrophage Maintenance and Homeostasis.Journal of immunology (Baltimore, Md. : 1950) · 2022Article
- Osteopontin aggravates acute lung injury in influenza virus infection by promoting macrophages necroptosis.Cell death discovery · 2022Article
- Common genetic aspects between COVID-19 and sarcoidosis: A network-based approach using gene expression data.Biochemistry and biophysics reports · 2022Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
Neutrophils are vital for antimicrobial defense; however, their role during viral infection is less clear. Furthermore, the molecular regulation of neutrophil fate and function at the viral infected sites is largely elusive. Here we report that BCL6 deficiency in myeloid cells exhibited drastically enhanced host resistance to severe influenza A virus (IAV) infection. In contrast to the notion that BCL6 functions to suppress innate inflammation, we find that myeloid BCL6 deficiency diminished lung inflammation without affecting viral loads. Using a series of Cre-transgenic, reporter, and knockout mouse lines, we demonstrate that BCL6 deficiency in neutrophils, but not in monocytes or lung macrophages, attenuated host inflammation and morbidity following IAV infection. Mechanistically, BCL6 bound to the neutrophil gene loci involved in cellular apoptosis in cells specifically at the site of infection. As such, BCL6 disruption resulted in increased expression of apoptotic genes in neutrophils in the respiratory tract, but not in the circulation or bone marrow. Consequently, BCL6 deficiency promoted tissue neutrophil apoptosis. Partial neutrophil depletion led to diminished pulmonary inflammation and decreased host morbidity. Our results reveal a previously unappreciated role of BCL6 in modulating neutrophil apoptosis at the site of infection for the regulation of host disease development following viral infection. Furthermore, our studies indicate that tissue-specific regulation of neutrophil survival modulates host inflammation and tissue immunopathology during acute respiratory viral infection.
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