Essential Role of Nuclear Factor κB in the Induction of Eosinophilia in Allergic Airway Inflammation

The molecular mechanisms that contribute to an eosinophil-rich airway inflammation in asthma are unclear. A predominantly T helper 2 (Th2)-type cell response has been documented in allergic asthma. Here we show that mice deficient in the p50 subunit of nuclear factor (NF)- κB are incapable of mounti...

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Main Authors:	Yang, Liyan, Cohn, Lauren, Zhang, Dong-Hong, Homer, Robert, Ray, Anuradha, Ray, Prabir
Format:	Online
Language:	English
Published:	The Rockefeller University Press 1998
Online Access:	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2212522/

id	pubmed-2212522
recordtype	oai_dc
spelling	pubmed-22125222008-04-16 Essential Role of Nuclear Factor κB in the Induction of Eosinophilia in Allergic Airway Inflammation Yang, Liyan Cohn, Lauren Zhang, Dong-Hong Homer, Robert Ray, Anuradha Ray, Prabir Articles The molecular mechanisms that contribute to an eosinophil-rich airway inflammation in asthma are unclear. A predominantly T helper 2 (Th2)-type cell response has been documented in allergic asthma. Here we show that mice deficient in the p50 subunit of nuclear factor (NF)- κB are incapable of mounting eosinophilic airway inflammation compared with wild-type mice. This deficiency was not due to a block in T cell priming or proliferation in the p50−/− mice, nor was it due to a defect in the expression of the cell adhesion molecules VCAM-1 and ICAM-1 that are required for the extravasation of eosinophils into the airways. The major defects in the p50−/− mice were the lack of production of the Th2 cytokine interleukin 5 and the chemokine eotaxin, which are crucial for proliferation and for differentiation and recruitment, respectively, of eosinophils into the asthmatic airway. Additionally, the p50−/− mice were deficient in the production of the chemokines macrophage inflammatory protein (MIP)-1α and MIP-1β that have been implicated in T cell recruitment to sites of inflammation. These results demonstrate a crucial role for NF-κB in vivo in the expression of important molecules that have been implicated in the pathogenesis of asthma. The Rockefeller University Press 1998-11-02 /pmc/articles/PMC2212522/ /pubmed/9802985 Text en This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/).
repository_type	Open Access Journal
institution_category	Foreign Institution
institution	US National Center for Biotechnology Information
building	NCBI PubMed
collection	Online Access
language	English
format	Online
author	Yang, Liyan Cohn, Lauren Zhang, Dong-Hong Homer, Robert Ray, Anuradha Ray, Prabir
spellingShingle	Yang, Liyan Cohn, Lauren Zhang, Dong-Hong Homer, Robert Ray, Anuradha Ray, Prabir Essential Role of Nuclear Factor κB in the Induction of Eosinophilia in Allergic Airway Inflammation
author_facet	Yang, Liyan Cohn, Lauren Zhang, Dong-Hong Homer, Robert Ray, Anuradha Ray, Prabir
author_sort	Yang, Liyan
title	Essential Role of Nuclear Factor κB in the Induction of Eosinophilia in Allergic Airway Inflammation
title_short	Essential Role of Nuclear Factor κB in the Induction of Eosinophilia in Allergic Airway Inflammation
title_full	Essential Role of Nuclear Factor κB in the Induction of Eosinophilia in Allergic Airway Inflammation
title_fullStr	Essential Role of Nuclear Factor κB in the Induction of Eosinophilia in Allergic Airway Inflammation
title_full_unstemmed	Essential Role of Nuclear Factor κB in the Induction of Eosinophilia in Allergic Airway Inflammation
title_sort	essential role of nuclear factor κb in the induction of eosinophilia in allergic airway inflammation
description	The molecular mechanisms that contribute to an eosinophil-rich airway inflammation in asthma are unclear. A predominantly T helper 2 (Th2)-type cell response has been documented in allergic asthma. Here we show that mice deficient in the p50 subunit of nuclear factor (NF)- κB are incapable of mounting eosinophilic airway inflammation compared with wild-type mice. This deficiency was not due to a block in T cell priming or proliferation in the p50−/− mice, nor was it due to a defect in the expression of the cell adhesion molecules VCAM-1 and ICAM-1 that are required for the extravasation of eosinophils into the airways. The major defects in the p50−/− mice were the lack of production of the Th2 cytokine interleukin 5 and the chemokine eotaxin, which are crucial for proliferation and for differentiation and recruitment, respectively, of eosinophils into the asthmatic airway. Additionally, the p50−/− mice were deficient in the production of the chemokines macrophage inflammatory protein (MIP)-1α and MIP-1β that have been implicated in T cell recruitment to sites of inflammation. These results demonstrate a crucial role for NF-κB in vivo in the expression of important molecules that have been implicated in the pathogenesis of asthma.
publisher	The Rockefeller University Press
publishDate	1998
url	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2212522/
_version_	1611434258029608960

Essential Role of Nuclear Factor κB in the Induction of Eosinophilia in Allergic Airway Inflammation

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