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Cited by 237Respiratory viral infections researchNF-κB Signaling PathwaysImmune Response and Inflammation

Respiratory Syncytial Virus–Induced Activation of Nuclear Factor–κB in the Lung Involves Alveolar Macrophages and Toll‐Like Receptor 4–Dependent Pathways

Haeberle, Helene A., Takizawa, Ryuta, Casola, Antonella, Brasier, Allan R., Dieterich, Hans‐Juergen, van Rooijen, Nico, Gatalica, Zoran, Garofalo, Roberto P.·2002·The Journal of Infectious Diseases
DOI 10.1086/344644
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Abstract

The transcription factor nuclear factor (NF)-kappaB controls the expression of numerous respiratory syncytial virus (RSV)-inducible inflammatory and immunomodulatory genes. Using a BALB/c mouse model, the present article shows that RSV potently and specifically activates NF-kappaB in vivo, a process that involves nuclear translocation of the subunits RelA, p50, and c-Rel in the lung. By depletion of alveolar macrophages (AMs) in BALB/c mice and use of C3H/HeJ mice lacking a functional Toll-like receptor (TLR)-4 signaling pathway, we demonstrate the existence of distinct but sequentially integrated RSV-inducible early NF-kappaB responses in the lung. The first response occurs early after RSV inoculation, is AM and TLR4 dependent, and is viral replication independent, whereas the second response involves epithelial cells and/or inflammatory cells, is TLR4 independent, and requires viral replication. NF-kappaB may be considered a central activator of not only inflammatory but also innate immune responses to RSV.

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Crossref · 10.1086/344644

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  • RSV induces Pseudomonas aeruginosa, S. pneumoniae, and H. influenzae adherence to airway epithelial cells.

    “RSV was shown to induce Pseudomonas aeruginosa, S. pneumoniae, and H. influenzae adherence to airway epithelial cells (12, 70, 95, 292)”

    From The airway epithelium: soldier in the fight against respiratory viruses (2011) · cites this paper as [95]

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Authors
Haeberle, H. A., Takizawa, R., Casola, A., Brasier, A. R., Dieterich, H., van Rooijen, N., Gatalica, Z., & Garofalo, R. P.
Affiliations
  • Universitätsklinikum Tübingen (DE)
  • Pediatrics and Genetics (US)
ORCID
Venue
The Journal of Infectious Diseases
Publisher
Oxford University Press (OUP)
Published
2002-11
Volume
186
Issue
9
Pages
1199-1206
ISSN
  • 0022-1899 (ISSN-L)
  • 1537-6613
DOI
10.1086/344644
OpenAlex
W2101292818
Cited by
237
References
42
Citations by year
2026: 4 · 2025: 8 · 2024: 2 · 2023: 6 · 2022: 6 · 2021: 4 · 2020: 5 · 2019: 5 · 2018: 8 · 2017: 13 · 2016: 4 · 2015: 6 · 2014: 14 · 2013: 11 · 2012: 9
FWCI
12.31
Type
journal article
Language
en
Open access
closed
Locations
  • The Journal of Infectious Diseases (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health (5r01ai015939-17, 5p01ai046004-04)
  • National Institute of Allergy and Infectious Diseases (AI46004, AI 15939)
Topics
  • Health Sciences › Medicine › Epidemiology › Respiratory viral infections research
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
  • Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
Keywords
respiratory syncytial virus, NF-κB activation, alveolar macrophages, TLR4, lung innate immunity, p65 nuclear translocation, epithelial cells, C3H/HeJ mice, BALB/c mouse model
MeSH terms
Animals, Humans, Lung, Membrane Glycoproteins, Mice, Inbred BALB C, Mice, Inbred C3H, Receptors, Cell Surface, Respiratory Syncytial Viruses, NF-kappa B, Macrophages, Alveolar, Respiratory Syncytial Virus Infections, Protein Subunits, Drosophila Proteins, Toll-Like Receptors, Toll-Like Receptor 4, Mice

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