ArticleLife science alliance2023
The pro-inflammatory response to influenza A virus infection is fueled by endothelial cells.
Article in Life science alliance, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.
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Who cites it
22 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.
- Lung Organoids: Systematic Review of Recent Advancements and its Future Perspectives.Tissue engineering and regenerative medicine · 2024Pooled it
- Predictive value of the prognostic nutritional index and aggregate index of systemic inflammation for pulmonary complications in children with influenza.Translational pediatrics · 2026Article
- Neutrophil myeloperoxidase as a functional biomarker for RSV severity: implications for in vitro therapeutic screening.Nature communications · 2026Article
- Article
- Dissecting Cell Death Pathways in Influenza A Virus Infection: Comparative Insights from Human Models.Viruses · 2026Review
- The expanding H5N1 avian influenza panzootic causes high mortality of skuas in Antarctica.Scientific reports · 2026Article
- Virus-induced endothelial senescence as a cause and driving factor for ME/CFS and long COVID: mediated by a dysfunctional immune system.Cell death & disease · 2026Review
- Pathology and virology of natural high pathogenicity avian influenza A(H5N1) Gs/GD genotype BB virus infection in wild black-headed gulls (Chroicocephalus ridibundus).Veterinary research · 2025Article
- Lung cell fates during influenza.Cell research · 2025Review
- Induction of tunnelling nanotube-like structures by influenza A viruses requires the onset of apoptosis.PLoS pathogens · 2025Article
- Pathogenesis Induced by Influenza Virus Infection: Role of the Early Events of the Infection and the Innate Immune Response.Viruses · 2025Review
- Long-term culture of chicken tracheal organoids for the purpose of avian influenza virus research.Virology journal · 2025Article
- Article
- Comparison of air-liquid interface transwell and airway organoid models for human respiratory virus infection studies.Frontiers in immunology · 2025Article
- Neurogenesis decreases in the offspring of mothers infected with influenza A virus.Frontiers in cellular and infection microbiology · 2025Article
- Viral-associated septic shock in pediatric pneumonia: a retrospective analysis of pathogen-specific risks and comparative clinical features with bacterial sepsis.Frontiers in pediatrics · 2025Article
- The Role of Inflammation in the Pathogenesis of Viral Respiratory Infections.Microorganisms · 2024Review
- Article
- Abortive Infection of Animal Cells: What Goes Wrong.Annual review of virology · 2024Review
- Examining longitudinal associations between prenatal exposure to infections and child brain morphology.Brain, behavior, and immunity · 2024Article
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
Morbidity and mortality from influenza are associated with high levels of systemic inflammation. Endothelial cells play a key role in systemic inflammatory responses during severe influenza A virus (IAV) infections, despite being rarely infected in humans. How endothelial cells contribute to systemic inflammatory responses is unclear. Here, we developed a transwell system in which airway organoid-derived differentiated human lung epithelial cells were co-cultured with primary human lung microvascular endothelial cells (LMECs). We compared the susceptibility of LMECs to pandemic H1N1 virus and recent seasonal H1N1 and H3N2 viruses and assessed the associated pro-inflammatory responses. Despite the detection of IAV nucleoprotein in LMEC mono-cultures, there was no evidence for productive infection. In epithelial-endothelial co-cultures, abundant IAV infection of epithelial cells resulted in the breakdown of the epithelial barrier, but infection of LMECs was rarely detected. We observed a significantly higher secretion of pro-inflammatory cytokines in LMECs when co-cultured with IAV-infected epithelial cells than LMEC mono-cultures exposed to IAV. Taken together, our data show that LMECs are abortively infected by IAV but can fuel the inflammatory response.
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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.