ArticleAmerican journal of respiratory cell and molecular biology2010
MCP-1 antibody treatment enhances damage and impedes repair of the alveolar epithelium in influenza pneumonitis.
Article in American journal of respiratory cell and molecular biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.
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Who cites it
67 citing papers in PubMed, 99 citations in OpenAlex.
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- Inflammatory, transcriptomic, and cell fate responses underlying the mammalian transmission of avian influenza viruses.Journal of virology · 2025Article
- Peripheral blood cytokine expression levels and their clinical significance in children with influenza.Translational pediatrics · 2025Article
- circ-0001454 alleviates asthma airway inflammation and remodeling via sponging miR-770-5p and regulating cbl-b.Frontiers in cell and developmental biology · 2025Article
- The role of alveolar macrophages in viral respiratory infections and their therapeutic implications.Biochemistry and biophysics reports · 2024Review
- The journey of SARS-CoV-2 in human hosts: a review of immune responses, immunosuppression, and their consequences.Virulence · 2021Review
- Granulocyte macrophage colony-stimulating factor has come of age: From a vaccine adjuvant to antiviral immunotherapy.Cytokine & growth factor reviews · 2021Review
- Administration of a CXC Chemokine Receptor 2 (CXCR2) Antagonist, SCH527123, Together with Oseltamivir Suppresses NETosis and Protects Mice from Lethal Influenza and Piglets from Swine-Influenza Infection.The American journal of pathology · 2021Article
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- A Novel Anti-Infective Peptide BCCY-1 With Immunomodulatory Activities.Frontiers in immunology · 2021Article
- The Many Faces of JAKs and STATs Within the COVID-19 Storm.Frontiers in immunology · 2021Review
- KScientific reports · 2020Article
- Diversity of locally produced IFN-α subtypes in human nasopharyngeal epithelial cells and mouse lung tissues during influenza virus infection.Applied microbiology and biotechnology · 2020Article
- Respiratory Barrier as a Safeguard and Regulator of Defense Against Influenza A Virus andFrontiers in immunology · 2020Review
- Abdominal and Pelvic Organ Failure Induced by Intraperitoneal Influenza A Virus Infection in Mice.Frontiers in microbiology · 2020Article
- Production of Neutrophil Extracellular Traps Contributes to the Pathogenesis ofFrontiers in immunology · 2020Article
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- Monocyte Chemoattractant Protein-1, a Possible Biomarker of Multiorgan Failure and Mortality in Ventilator-Associated Pneumonia.International journal of molecular sciences · 2019Article
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- The Role of Matrix Protein 2 Ectodomain in the Development of Universal Influenza Vaccines.The Journal of infectious diseases · 2019Article
7 more citing papers are in PubMed but not listed here.
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recent studies have demonstrated an essential role of alveolar macrophages during influenza virus infection. Enhanced mortalities were observed in macrophage-depleted mice and pigs after influenza virus infection, but the basis for the enhanced pathogenesis is unclear. This study revealed that blocking macrophage recruitment into the lungs in a mouse model of influenza pneumonitis resulted in enhanced alveolar epithelial damage and apoptosis, as evaluated by histopathology, immunohistochemistry, Western blot, RT-PCR, and TUNEL assays. Abrogation of macrophage recruitment was achieved by treatment with monoclonal antibody against monocyte chemoattractant protein-1 (MCP-1) after sub-lethal challenge with mouse-adapted human influenza A/Aichi/2/68 virus. Interestingly, elevated levels of hepatocyte growth factor (HGF), a mitogen for alveolar epithelium, were detected in bronchoalveolar lavage samples and in lung homogenates of control untreated and nonimmune immunoglobulin (Ig)G-treated mice after infection compared with anti-MCP-1-treated infected mice. The lungs of control animals also displayed strongly positive HGF staining in alveolar macrophages as well as alveolar epithelial cell hyperplasia. Co-culture of influenza virus-infected alveolar epithelial cells with freshly isolated alveolar macrophages induced HGF production and phagocytic activity of macrophages. Recombinant HGF added to mouse lung explants after influenza virus infection resulted in enhanced BrdU labeling of alveolar type II epithelial cells, indicating their proliferation, in contrast with anti-HGF treatment showing significantly reduced epithelial regeneration. Our data indicate that inhibition of macrophage recruitment augmented alveolar epithelial damage and apoptosis during influenza pneumonitis, and that HGF produced by macrophages in response to influenza participates in the resolution of alveolar epithelium.
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