ArticlePloS one2022
M1-like, but not M0- or M2-like, macrophages, reduce RSV infection of primary bronchial epithelial cells in a media-dependent fashion.
Article in PloS one, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
10 citing papers in PubMed, 13 citations in OpenAlex.
- Suppression of Nr1d1/Bnip3-dependent mitophagy by notch signaling aggravates inflammatory response in RSV-infected mice lungs.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Particle dissolution rate controls macrophage response and drug release from mesoporous silica inhalation carriers.Scientific reports · 2026Article
- Review
- Review
- Cordycepin, lactoferrin, and Sargassum fusiforme polysaccharides protects against RSV via M2-like macrophage polarization.Frontiers in immunology · 2025Article
- Development of an intestinal mucosaJournal of virology · 2024Article
- Transcriptome profiling of macrophages persistently infected with human respiratory syncytial virus and effect of recombinantFrontiers in microbiology · 2024Article
- On the path to predicting immune responses in the lung: Modeling the pulmonary innate immune system at the air-liquid interface (ALI).European journal of pharmaceutical sciences : official journal of the European Federation for Pharmaceutical Sciences · 2023Review
- Air-Liquid interface cultures to model drug delivery through the mucociliary epithelial barrier.Advanced drug delivery reviews · 2023Review
- Development of innate and adaptive immunity to RSV in young children.Cellular immunologyReview
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Respiratory syncytial virus (RSV) is a common childhood infection that in young infants can progress into severe bronchiolitis and pneumonia. Disease pathogenesis results from both viral mediated and host immune processes of which alveolar macrophages play an important part. Here, we investigated the role of different types of alveolar macrophages on RSV infection using an in vitro co-culture model involving primary tissue-derived human bronchial epithelial cells (HBECs) and human blood monocyte-derived M0-like, M1-like, or M2-like macrophages. It was hypothesized that the in vitro model would recapitulate previous in vivo findings of a protective effect of macrophages against RSV infection. It was found that macrophages maintained their phenotype for the 72-hour co-culture time period and the bronchial epithelial cells were unaffected by the macrophage media. HBEC infection with RSV was decreased by M1-like macrophages but enhanced by M0- or M2-like macrophages. The medium used during the co-culture also impacted the outcome of the infection. This work demonstrates that alveolar macrophage phenotypes may have differential roles during epithelial RSV infection, and demonstrates that an in vitro co-culture model could be used to further investigate the roles of macrophages during bronchial viral infection.
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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 Socratic graph.