ArticleFrontiers in immunology2022
Autophagy and Exosome Coordinately Enhance Macrophage M1 Polarization and Recruitment in Influenza A Virus Infection.
Article in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 31 citations in OpenAlex.
- Dual-function cytokines as modulators of autophagy: reprogramming inflammatory resolution in severe COVID-19.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
- Article
- Exosomes in inflammatory tissue injury: key pathogenic factors and promising therapeutic agents.Frontiers in immunology · 2026Review
- Advances in understanding exosome-mediated regulation of macrophage function.Frontiers in immunology · 2026Review
- A novel C-3-substituted oleanolic acid benzyl amide derivative exhibits therapeutic potential against influenza A by targeting PA-PB1 interactions and modulating host macrophage inflammation.Acta pharmaceutica Sinica. B · 2025Article
- Changes and application prospects of biomolecular materials in small extracellular vesicles (sEVs) after flavivirus infection.European journal of medical research · 2025Review
- Autophagy and Respiratory Viruses: Mechanisms, Viral Exploitation, and Therapeutic Insights.Cells · 2025Review
- Influenza, SARS-CoV-2, and Their Impact on Chronic Lung Diseases and Fibrosis: Exploring Therapeutic Options.The American journal of pathology · 2024Review
- IRF3 inhibits inflammatory signaling pathways in macrophages to prevent viral pathogenesis.Science advances · 2024Article
- Baicalin reduced injury of and autophagy-related gene expression in RAW264.7 cells infected with H6N6 avian influenza virus.Heliyon · 2024Article
- Extracellular vesicles and endothelial dysfunction in infectious diseases.Journal of extracellular biology · 2024Review
- Exosomes derived from programmed cell death: mechanism and biological significance.Cell communication and signaling : CCS · 2024Review
- The Roles of Endocytosis and Autophagy at the Cellular Level During Influenza Virus Infection: A Mini-Review.Infection and drug resistance · 2024Review
- Extracellular Vesicles and Their Role in Lung Infections.International journal of molecular sciences · 2023Review
- Total Osteopontin and Its Isoform OPN4 Are Differently Expressed in Respiratory Samples during Influenza A(H1N1)pdm09 Infection and Progression.Microorganisms · 2023Article
- Article
- Article
- Impact of extracellular vesicles on the pathogenesis, diagnosis, and potential therapy in cardiopulmonary disease.Frontiers in pharmacology · 2023Review
- Diverse roles of lung macrophages in the immune response to influenza A virus.Frontiers in microbiology · 2023Review
- Role of Ceramides and Lysosomes in Extracellular Vesicle Biogenesis, Cargo Sorting and Release.International journal of molecular sciences · 2022Review
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Influenza A virus infection results in viral pneumonia, which is often accompanied by the infiltration and recruitment of macrophages, overactivation of inflammatory responses, and obvious cell autophagy and exosome production. However, little is known about the roles of autophagy and exosome production in these inflammatory responses. Methods: In this study, multiple methods, such as flow cytometry, real-time quantitative reverse transcription-polymerase chain reaction, immune-fluorescence technology, and western blot, were applied to explore the possible effects of autophagy and exosome production by H1N1-infected host cells. Results: It was observed that a high number of polarized macrophages (CD11b Conclusion: Autophagy and exosome production coordinately enhance the M1 polarization and recruitment of macrophages in influenza virus infection, which also provides potential therapeutic targets.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.