Abstract
The transcription factor nuclear factor (NF)-κB 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-κB 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-κB 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-κB may be considered a central activator of not only inflammatory but also innate immune responses to RSV.
| Original language | English |
|---|---|
| Pages (from-to) | 1199-1206 |
| Number of pages | 8 |
| Journal | Journal of Infectious Diseases |
| Volume | 186 |
| Issue number | 9 |
| DOIs | |
| State | Published - Nov 1 2002 |
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ASJC Scopus subject areas
- Public Health, Environmental and Occupational Health
- Immunology
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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.
In: Journal of Infectious Diseases, Vol. 186, No. 9, 01.11.2002, p. 1199-1206.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Respiratory syncytial virus-induced activation of nuclear factor-κB in the lung involves alveolar macrophages and toll-like receptor 4-dependent pathways
AU - Haeberle, Helene A.
AU - Takizawa, Ryuta
AU - Casola, Antonella
AU - Brasier, Allan R.
AU - Dieterich, Hans Juergen
AU - Van Rooijen, Nico
AU - Gatalica, Zoran
AU - Garofalo, Roberto
PY - 2002/11/1
Y1 - 2002/11/1
N2 - The transcription factor nuclear factor (NF)-κB 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-κB 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-κB 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-κB may be considered a central activator of not only inflammatory but also innate immune responses to RSV.
AB - The transcription factor nuclear factor (NF)-κB 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-κB 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-κB 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-κB may be considered a central activator of not only inflammatory but also innate immune responses to RSV.
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UR - http://www.scopus.com/inward/citedby.url?scp=0036838764&partnerID=8YFLogxK
U2 - 10.1086/344644
DO - 10.1086/344644
M3 - Article
C2 - 12402188
AN - SCOPUS:0036838764
VL - 186
SP - 1199
EP - 1206
JO - Journal of Infectious Diseases
JF - Journal of Infectious Diseases
SN - 0022-1899
IS - 9
ER -