Skip header and navigation

1 records – page 1 of 1.

Adoptive transfer of alveolar macrophages abrogates bronchial hyperresponsiveness.

https://arctichealth.org/en/permalink/ahliterature15196
Source
Am J Respir Cell Mol Biol. 2004 Jul;31(1):22-7
Publication Type
Article
Date
Jul-2004
Author
Eric Careau
Elyse Y Bissonnette
Author Affiliation
Centre de Recherche, Hôpital Laval, Institut universitaire de Cardiologie et de Pneumologie de l'Université Laval, Québec, Canada. eric.careau@crhl.ulaval.ca
Source
Am J Respir Cell Mol Biol. 2004 Jul;31(1):22-7
Date
Jul-2004
Language
English
Publication Type
Article
Keywords
Adoptive Transfer
Animals
Asthma - physiopathology
Bronchi - drug effects - immunology - physiopathology
Bronchial Hyperreactivity - genetics - physiopathology - therapy
Bronchial Provocation Tests
Clodronic Acid
Disease Models, Animal
Dose-Response Relationship, Drug
Drug Resistance - physiology
Genetic Predisposition to Disease - genetics
Immunoglobulin E - blood
Immunoglobulin G - blood
Liposomes
Macrophages, Alveolar - drug effects - immunology - transplantation
Male
Methacholine Chloride - pharmacology
Ovalbumin - immunology
Rats
Rats, Sprague-Dawley
Reaction Time - drug effects - physiology
Research Support, Non-U.S. Gov't
Abstract
Increasing evidence suggests that alveolar macrophages (AM) are involved in asthma pathogenesis. To better understand the role that these cells play, we investigated the capacity of AM from allergy-resistant rat, Sprague Dawley (SD), to modulate airway hyperresponsiveness of allergy-susceptible rat, Brown Norway (BN). AM of ovalbumin (OVA)-sensitized BN rats were eliminated by intratracheal instillation of liposomes containing clodronate. AM from OVA-sensitized SD rats were transferred into AM-depleted BN rats 24 h before allergen challenge. Airway responsiveness to methacholine was measured the following day. Instillation of liposomes containing clodronate in BN rats eliminated 85% AM after 3 d compared with saline liposomes. Methacholine concentration needed to increase lung resistance by 200% (EC200RL) was significantly lower in OVA-challenged BN rats (27.9 +/- 2.8 mg/ml) compared with SD rats (63.9 +/- 8.6 mg/ml). However, when AM from SD rats were transferred into AM-depleted BN rats, airway responsiveness (64.0 +/- 11.3 mg/ml) was reduced to the level of naïve rats (54.4 +/- 3.7 mg/ml) in a dose-dependent manner. Interestingly, transfer of AM from BN rats into SD rats did not modulate airway responsiveness. To our knowledge, this is the first direct evidence showing that AM may protect against the development of airway hyperresponsiveness.
Notes
Comment In: Am J Respir Cell Mol Biol. 2004 Jul;31(1):1-215208095
Comment In: Am J Respir Cell Mol Biol. 2004 Jul;31(1):3-715208096
PubMed ID
14962974 View in PubMed
Less detail