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Mice Lacking Epithelial I-?B Kinase are Protected from Lipopolysaccharide and Cigarette Smoke Extract Induced Inflammation | OMICS International | Abstract
ISSN: 2161-105X

Journal of Pulmonary & Respiratory Medicine
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Research Article

Mice Lacking Epithelial I-?B Kinase are Protected from Lipopolysaccharide and Cigarette Smoke Extract Induced Inflammation

David Lamb1*, Nicole Parker1, Kristina Ulrich1, Gareth Jones2, Coralie Afeldorfer2, Manolis Pasparakis3, Steven Evans1, and Iain Kilty1

1Allergy and Respiratory Research Unit, Pfizer Research Laboratories, UK

2Drug Safety Research and Development, Pfizer Research Laboratories, UK

3Institute for Genetics, Zülpicher Strasse 47a, D-50674 Cologne, Germany

*Corresponding Author:
David Lamb
Allergy and Respiratory Research Unit
Pfizer Research Laboratories
Pfizer (UK) Ltd, Ramsgate Road
Sandwich, Kent, CT13 9NJ, UK
E-mail: [email protected]

Received date: January 30, 2013; Accepted date: February 20, 2013; Published date: February 25, 2013

Citation: Lamb D, Parker N, Ulrich K, Jones G, Afeldorfer C, et al. (2013) Mice Lacking Epithelial I-?B Kinase are Protected from Lipopolysaccharide and Cigarette Smoke Extract Induced Inflammation. J Pulmon Resp Med 3:142. doi:10.4172/2161-105X.1000142

Copyright: © 2013 Lamb D, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Background: IKK-2 activity is essential for cytokine mediated NFκB activation and subsequent expression of a wide variety of inflammatory genes. To investigate the role of IKK-2 signalling in lung epithelium we have developed a knock out mouse in which we have specifically deleted the IKK-2 gene in lung epithelial cells.

Materials and Methods: IKK-2 KO mice and littermate control animals were challenged with either nebulised Lipopolysaccharide (LPS) or with Cigarette Smoke Extract (CSE). Cytokines and inflammatory cells were assessed in Bronchoalveolar Lavage Fluid (BALF) and tissue inflammatory cells, markers of apoptosis and general pathology assessed histologically.

Results: BALF neutrophils were reduced by 63% at 4 hours and 67% at 8 hours following LPS challenge in the IKK-2 KO animals (P<0.001). Immunocytochemical analysis showed no difference in neutrophil numbers within pulmonary tissue between the groups or any evidence of increased apoptosis. BALF neutrophils were also reduced below control values in the IKK-2 KO mice in response to CSE compared to littermates animals (P<0.005).

Conclusion: Mice lacking IKK-2 in the pulmonary epithelium recruit fewer neutrophils into the airways in response to both LPS and CSE challenge, suggesting that the epithelium participates in airway inflammatory neutrophil recruitment in response to inflammatory challenge.

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