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Table of Contents
Vol. 160, No. 2, 2013
Issue release date: January 2013
Section title: Original Paper
Int Arch Allergy Immunol 2013;160:173–183
(DOI:10.1159/000341645)

Biphasic Late Airway Hyperresponsiveness in a Murine Model of Asthma

Kim H.-K.a · Lee C.-H.a · Kim J.-M.a · Ayush O.a · Im S.-Y.b · Lee H.-K.a
aDepartment of Immunology, Chonbuk National University Medical School, Jeonju, and bDepartment of Biological Sciences, College of Natural Sciences, Chonnam National University, Gwangju, Republic of Korea

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Article / Publication Details

First-Page Preview
Abstract of Original Paper

Received: April 10, 2012
Accepted: July 06, 2012
Published online: September 25, 2012
Issue release date: January 2013

Number of Print Pages: 11
Number of Figures: 5
Number of Tables: 0

ISSN: 1018-2438 (Print)
eISSN: 1423-0097 (Online)

For additional information: http://www.karger.com/IAA

Abstract

Background: Nonspecific airway hyperresponsiveness (AHR) is one of the cardinal features of bronchial asthma. Early AHR is caused by chemical mediators released from pulmonary mast cells activated in an IgE-dependent way. However, the mechanism of late AHR remains unclear. Methods: Features of airway allergic inflammation were analyzed, including antigen-induced AHR, using a murine model of asthma. The model was suitable for examining the sequential early molecular events occurring after the initial airway exposure to antigen. Results: AHR increased at 10–12 h after airway challenge, followed by the second-phase response, which was larger and broader in resistance at 18–30 h. Pretreatment of sensitized animals with anti-tumor necrosis factor (TNF) before airway challenge or induction of allergic asthma in TNF–/– mice resulted in abrogation of the first-phase late AHR. Intratracheal instillation of TNF induced a single peak of AHR at 10 h. IgE and IgG immune complexes induced the development of the first-phase late AHR by TNF production. Pretreatment with cytosolic phospholipase inhibitor and 5-lipoxygenase inhibitors abolished the first-phase late AHR as well as the leukotriene B4 levels in the airway. CpG-oligodeoxynucleotide (ODN) pretreatment reduced airway levels of Th2 cytokines, eosinophil infiltration and second-phase late AHR. However, CpG-ODN did not reduce TNF levels or the magnitude of first-phase late AHR. Conclusion: Biphasic late AHR occurs in a murine model of asthma. First- and second-phase late AHR is caused by TNF and Th2 response, respectively.

© 2012 S. Karger AG, Basel


Article / Publication Details

First-Page Preview
Abstract of Original Paper

Received: April 10, 2012
Accepted: July 06, 2012
Published online: September 25, 2012
Issue release date: January 2013

Number of Print Pages: 11
Number of Figures: 5
Number of Tables: 0

ISSN: 1018-2438 (Print)
eISSN: 1423-0097 (Online)

For additional information: http://www.karger.com/IAA


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