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The effects of IL-5 on airway physiology and inflammation in rats.

https://arctichealth.org/en/permalink/ahliterature15276
Source
J Allergy Clin Immunol. 2003 Mar;111(3):558-66
Publication Type
Article
Date
Mar-2003
Author
Sammy S Nag
Li Jing Xu
Qutayba Hamid
Paolo M Renzi
Author Affiliation
CHUM Research Center, Notre Dame Pavillion, University of Montreal, and the Meakins-Christie Laboratories, McGill University, Quebec, Canada.
Source
J Allergy Clin Immunol. 2003 Mar;111(3):558-66
Date
Mar-2003
Language
English
Publication Type
Article
Keywords
Animals
Blood Cells - pathology
Bronchoalveolar Lavage Fluid - cytology
Cell Differentiation - drug effects
Cytokines - genetics
Dose-Response Relationship, Drug
Eosinophils - pathology
Humans
Immunization
Immunoglobulin E - blood
Inflammation - physiopathology
Interleukin-5 - administration & dosage - pharmacology
Intubation, Intratracheal
Lung - metabolism
Lymphocyte Subsets - pathology
Male
Methacholine Chloride - pharmacology
Ovalbumin - immunology
RNA, Messenger - metabolism
Rats
Rats, Inbred BN
Recombinant Proteins - administration & dosage - pharmacology
Research Support, Non-U.S. Gov't
Respiratory System - drug effects - physiopathology
Respiratory Tract Diseases - physiopathology
Stem Cells - pathology
Abstract
BACKGROUND: There is evidence that the cytokine IL-5 is a prominent feature of airway inflammation in asthma. OBJECTIVE: The aim of this study was to determine whether exogenous IL-5 could cause changes in lung physiology, the early and late airway response after antigen challenge, and airway inflammation in rats that do not have a propensity to develop these changes after sensitization and challenge. METHOD AND RESULTS: Intratracheal administration of IL-5 to ovalbumin sensitized Brown Norway SSN rats increased the airway responsiveness to methacholine (AHR) 20 hours after administration of IL-5 at the same time as an increase in neutrophils occurred in the lung lavage. This effect was dose dependent and was not caused by endotoxin. Concurrent intratracheal administration of 50 ng of anti-IL-5 monoclonal antibody with 10 microg of recombinant human IL-5 decreased the AHR and neutrophil influx. Pretreatment with 3 microg of IL-5 had no effect on the early and late airway response or on AHR after ovalbumin challenge. However, IL-5 increased lung re-sistance 20 hours after antigen challenge. Although total lung cells and differential counts did not differ significantly 8 hours after antigen challenge, the blood lymphocyte CD4/CD8 ratio decreased in IL-5 pretreated rats (P
PubMed ID
12642837 View in PubMed
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Inhibition of antigen-induced eosinophilia and airway hyperresponsiveness by antisense oligonucleotides directed against the common beta chain of IL-3, IL-5, GM-CSF receptors in a rat model of allergic asthma.

https://arctichealth.org/en/permalink/ahliterature15390
Source
Am J Respir Crit Care Med. 2002 Apr 1;165(7):1015-21
Publication Type
Article
Date
Apr-1-2002
Author
Zoulfia Allakhverdi
Mustapha Allam
Paolo M Renzi
Author Affiliation
CHUM Research Center, Notre-Dame Hospital, University of Montreal, Montreal, Quebec, Canada.
Source
Am J Respir Crit Care Med. 2002 Apr 1;165(7):1015-21
Date
Apr-1-2002
Language
English
Publication Type
Article
Keywords
Animals
Antigens - immunology
Asthma - immunology - pathology - physiopathology
Bone Marrow Cells - metabolism
Bronchial Hyperreactivity
Cell Count
Cells, Cultured
Dose-Response Relationship, Drug
Eosinophils - pathology
Immunization
Leukotriene D4 - pharmacology
Lung - metabolism - pathology
Male
Oligonucleotides, Antisense - pharmacology
Ovalbumin - immunology
RNA, Messenger - metabolism
Rats
Rats, Inbred BN
Receptors, Granulocyte-Macrophage Colony-Stimulating Factor - chemistry - genetics - physiology
Receptors, Interleukin - chemistry - genetics - physiology
Receptors, Interleukin-3 - chemistry - genetics - physiology
Research Support, Non-U.S. Gov't
Transcription, Genetic
Abstract
Airway obstruction, hyperresponsiveness, and the accumulation and persistence within the airways of inflammatory cells characterize asthma. Interleukin (IL)-3, granulocyte macrophage colony- stimulating factor (GM-CSF), and IL-5 are among several cytokines that have been shown to be increased in asthma and to contribute to atopic inflammation. They mediate their effect via receptors that have a common beta subunit (beta(c)). We hypothesized that blocking of this common beta(c) would impair the airway response to antigen. We report that an antisense (AS) phosphorothioate oligodeoxynucleotide (ODN) found to specifically inhibit transcription of the beta(c) in rat bone marrow cells also caused inhibition of beta(c) mRNA expression and of immunoreactive cells within the lungs of Brown Norway (BN) rats when injected intratracheally (p
PubMed ID
11934731 View in PubMed
Less detail