NDLI: A Prominent Role for Airway Epithelial NF-κB Activation in Lipopolysaccharide-Induced Airway Inflammation

Please wait, while we are loading the content...

A Prominent Role for Airway Epithelial NF-κB Activation in Lipopolysaccharide-Induced Airway Inflammation

Content Provider	Scilit
Author	Poynter, Matthew E. Irvin, Charles G. Janssen-Heininger, Yvonne M. W.
Copyright Year	2003
Description	To reveal the causal role of airway epithelial NF-κB activation in evoking airway inflammation, a transgenic mouse was created expressing a mutant version of the inhibitory protein I-κBα. This I-κBα superrepressor $(I-κBα_{SR}$) acts to repress NF-κB activation exclusively in airway epithelial cells, under the transcriptional control of the rat CC10 promoter $(CC10-I-κBα_{SR}$). Compared with transgene-negative littermates, intranasal instillation of LPS did not induce nuclear translocation of NF-κB in airway epithelium of $CC10-I-κBα_{SR}$ transgenic mice. Consequently, the influx of neutrophils into the airways and secretion of the NF-κB-regulated neutrophilic chemokine, macrophage-inflammatory protein-2, and the inflammatory cytokine, TNF-α, were markedly reduced in $CC10-I-κBα_{SR}$ mice relative to the transgene-negative mice exposed to LPS. Despite an inability to activate NF-κB in airway epithelium, resident alveolar macrophages from transgene-positive mice were capable of activating NF-κB in a manner indistinguishable from transgene-negative mice. These findings demonstrate that airway epithelial cells play a prominent role in orchestrating the airway inflammatory response to LPS and suggest that NF-κB signaling in these cells is important for modulating innate immune responses to microbial products.
Ending Page	6265
Page Count	9
Starting Page	6257
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.170.12.6257
Journal	The Journal of Immunology
Issue Number	12
Volume Number	170
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2003-06-15
Access Restriction	Open
Subject Keyword	Innate Immune Nf Κb Activation Airway Epithelium Airway Epithelial Cells
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

Sl.	Authority	Responsibilities	Communication Details
1	Ministry of Education (GoI), Department of Higher Education	Sanctioning Authority	https://www.education.gov.in/ict-initiatives
2	Indian Institute of Technology Kharagpur	Host Institute of the Project: The host institute of the project is responsible for providing infrastructure support and hosting the project	https://www.iitkgp.ac.in
3	National Digital Library of India Office, Indian Institute of Technology Kharagpur	The administrative and infrastructural headquarters of the project	Dr. B. Sutradhar bsutra@ndl.gov.in
4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
5	Website/Portal (Helpdesk)	Queries regarding NDLI and its services	support@ndl.gov.in
6	Contents and Copyright Issues	Queries related to content curation and copyright issues	content@ndl.gov.in
7	National Digital Library of India Club (NDLI Club)	Queries related to NDLI Club formation, support, user awareness program, seminar/symposium, collaboration, social media, promotion, and outreach	clubsupport@ndl.gov.in
8	Digital Preservation Centre (DPC)	Assistance with digitizing and archiving copyright-free printed books	dpc@ndl.gov.in
9	IDR Setup or Support	Queries related to establishment and support of Institutional Digital Repository (IDR) and IDR workshops	idr@ndl.gov.in

Airway Epithelium Controls Lung Inflammation and Injury through the NF-κB Pathway

Airway Epithelial NF-κB Activation Modulates Asbestos-Induced Inflammation and Mucin Production In Vivo

Dual Role of NOX2 in Respiratory Syncytial Virus- and Sendai Virus-Induced Activation of NF-κB in Airway Epithelial Cells

Role of NF-κB in Cytokine Production Induced from Human Airway Epithelial Cells by Rhinovirus Infection

Targeted Immunomodulation of the NF-κB Pathway in Airway Epithelium Impacts Host Defense against Pseudomonas aeruginosa

A Role for NF-κB Subunits p50 and p65 in the Inhibition of Lipopolysaccharide-Induced Shock

Amygdalin Attenuates Airway Epithelium Apoptosis, Inflammation, and Epithelial-Mesenchymal Transition through Restraining the TLR4/NF-κB Signaling Pathway on LPS-Treated BEAS-2B Bronchial Epithelial Cells

Adenovirus 7 Induces Interlukin-6 Expression in Human Airway Epithelial Cells via p38/NF-κB Signaling Pathway

EBV-Induced Gene 3 Transcription Is Induced by TLR Signaling in Primary Dendritic Cells via NF-κB Activation

A Prominent Role for Airway Epithelial NF-κB Activation in Lipopolysaccharide-Induced Airway Inflammation

Similar Documents

Airway Epithelium Controls Lung Inflammation and Injury through the NF-κB Pathway

Airway Epithelial NF-κB Activation Modulates Asbestos-Induced Inflammation and Mucin Production In Vivo

Dual Role of NOX2 in Respiratory Syncytial Virus- and Sendai Virus-Induced Activation of NF-κB in Airway Epithelial Cells

Role of NF-κB in Cytokine Production Induced from Human Airway Epithelial Cells by Rhinovirus Infection

Targeted Immunomodulation of the NF-κB Pathway in Airway Epithelium Impacts Host Defense against Pseudomonas aeruginosa

A Role for NF-κB Subunits p50 and p65 in the Inhibition of Lipopolysaccharide-Induced Shock

Amygdalin Attenuates Airway Epithelium Apoptosis, Inflammation, and Epithelial-Mesenchymal Transition through Restraining the TLR4/NF-κB Signaling Pathway on LPS-Treated BEAS-2B Bronchial Epithelial Cells

Adenovirus 7 Induces Interlukin-6 Expression in Human Airway Epithelial Cells via p38/NF-κB Signaling Pathway

EBV-Induced Gene 3 Transcription Is Induced by TLR Signaling in Primary Dendritic Cells via NF-κB Activation

A Prominent Role for Airway Epithelial NF-κB Activation in Lipopolysaccharide-Induced Airway Inflammation