Title
Alveolar macrophages have a dual role in a rat model for trimellitic anhydride-induced occupational asthma
Author
Valstar, D.L.
Schijf, M.A.
Nijkamp, F.P.
Storm, G.
Arts, J.H.E.
Kuper, C.F.
Bloksma, N.
Henricks, P.A.J.
TNO Kwaliteit van Leven
Publication year
2006
Abstract
Occupational exposure to low molecular weight chemicals, like trimellitic anhydride (TMA), can result in occupational asthma. Alveolar macrophages (AMs) are among the first cells to encounter inhaled compounds. These cells can produce many different mediators that have a putative role in asthma. In this study, we examined the role of AMs in lung function and airway inflammation of rats exposed to TMA. Female Brown Norway rats were sensitized by dermal application of TMA or received vehicle alone on days 0 and 7. One day before challenge, rats received intratracheally either empty or clodronate-containing liposomes to deplete the lungs of AMs. On day 21, all rats were challenged by inhalation of TMA in air. Lung function parameters were measured before, during, within 1 h after, and 24 h after challenge. IgE levels and parameters of inflammation and tissue damage were assessed 24 h after challenge. Sensitization with TMA led to decreased lung function parameters during and within 1 h after challenge as compared to non-sensitized rats. AM depletion alleviated the TMA-induced drop in lung function parameters and induced a faster recovery compared to sham-depleted TMA-sensitized rats. It also decreased the levels of serum IgE 24 h after challenge, but did not affect the sensitization-dependent increase in lung lavage fluid IL-6 and tissue TNF-α levels. In contrast, AM depletion augmented the TMA-induced tissue damage and inflammation 24 h after challenge. AMs seem to have a dual role in this model for TMA-induced occupational asthma since they potentiate the immediate TMA-induced decrease in lung function but tended to dampen the TMA-induced inflammatory reaction 24 h later. © 2005 Elsevier Inc. All rights reserved.
Subject
Health
Toxicology and Applied Pharmacology
Airway inflammation
Alveolar macrophages
Early asthmatic response
Occupational asthma
Trimellitic anhydride
clodronic acid
immunoglobulin E
interleukin 6
liposome
trimellitic anhydride
tumor necrosis factor alpha
animal cell
animal experiment
animal model
animal tissue
article
body weight
cell function
controlled study
disease severity
female
immunoglobulin blood level
lung alveolus macrophage
lung function
lung injury
lung lavage
lymphocyte depletion
nonhuman
occupational asthma
organ weight
rat
respiratory tract inflammation
Allergens
Analysis of Variance
Animals
Asthma
Cytokines
Disease Models, Animal
Female
Immunoglobulin E
Lung
Macrophages, Alveolar
Occupational Diseases
Phthalic Anhydrides
Rats
Rats, Inbred BN
Respiratory Function Tests
Statistics, Nonparametric
Animalia
Rattus norvegicus
To reference this document use:
http://resolver.tudelft.nl/uuid:5cb7eae9-3ffa-4ec8-95de-467725f51a03
DOI
https://doi.org/10.1016/j.taap.2005.05.012
TNO identifier
239132
ISSN
0041-008X
Source
Toxicology and Applied Pharmacology, 211 (1), 20-29
Document type
article