Interleukin-2-induced Increased Airway Responsiveness and Lung Th2 Cytokine Expression Occur after Antigen Challenge through the Leukotriene Pathway

Previous studies have shown that the allergic late airway response (LR) is dependent on the leukotriene (LT) pathway in Brown Norway (BN) rats. In this same model, interleukin-2 (IL-2) has been shown to increase allergic airway responses without increasing LT production. This study examined the rela...

Full description

Saved in:
Bibliographic Details
Published in:American journal of respiratory and critical care medicine 2002-06, Vol.165 (11), p.1540-1545
Main Authors: Nag, Sammy, Lamkhioued, Bouchaib, Renzi, Paolo M
Format: Article
Language:English
Subjects:
Airway Resistance - drug effects
Airway Resistance - immunology
Allergic diseases
Analysis of Variance
Animals
Biological and medical sciences
Cytokines - immunology
Cytokines - metabolism
Disease Models, Animal
Immunity, Cellular - drug effects
Immunopathology
In Situ Hybridization
Interferon-gamma - analysis
Interferon-gamma - metabolism
Interleukin-2 - pharmacology
Leukotriene D4 - analysis
Leukotriene D4 - metabolism
Male
Medical sciences
Rats
Rats, Inbred BN
Reference Values
Respiratory and ent allergic diseases
Reverse Transcriptase Polymerase Chain Reaction
RNA, Messenger - analysis
Sensitivity and Specificity
Statistics, Nonparametric
Th2 Cells - immunology
Up-Regulation
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Previous studies have shown that the allergic late airway response (LR) is dependent on the leukotriene (LT) pathway in Brown Norway (BN) rats. In this same model, interleukin-2 (IL-2) has been shown to increase allergic airway responses without increasing LT production. This study examined the relationship between the upregulation of cellular immunity with IL-2 and the LT pathway in ovalbumin-sensitized BN rats. Airway responsiveness to LTD(4) was significantly increased in BN rats pretreated with IL-2 (20,000 U twice a day for 4.5 days). Treatment with montelukast, a cysteinyl LT(1) receptor antagonist, blocked IL-2's induced increase of the LR to ovalbumin challenge. When cytokine expression was assessed either by semiquantitative polymerase chain reaction or in situ hybridization, we found that montelukast decreased the amount of IL-4 mRNA expression in the lungs while increasing the amount of interferon-gamma mRNA expression 8 hours after challenge. These results indicate that upregulation of cellular immunity with IL-2 can increase the sensitivity of the airways to LTD(4) and that inhibition of the LT pathway will block the LR and modulate cytokine expression after antigen challenge.
ISSN:1073-449X
1535-4970
DOI:10.1164/rccm.2109012