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Measurement of the release of inflammatory mediators from rat alveolar macrophages and alveolar type II cells following lipopolysaccharide or silica exposure: a comparative study.

Authors
Kanj-RS; Kang-JL; Castranova-V
Source
J Toxicol Environ Health, A 2005 Feb; 68(3):185-207
NIOSHTIC No.
20025842
Abstract
Evidence suggests that hyperproduction of reactive oxidants and inflammatory mediators plays a critical role in adverse pulmonary responses to silica or lipopolysaccharide (LPS). The objective of this study was to evaluate the role of alveolar macrophages (AM) and alveolar epithelial type II cells (TII) in the induction of pulmonary inflammation and injury in response to these pulmonary toxicants. To support this objective, the release of several inflammatory mediators from primary rat AMs and TII cells was compared under similar culture and exposure conditions. The responsiveness of RLE-6TN, a rat type II cell line, was also compared to primary rat TII cells under the same culture conditions, following exposure to LPS or silica. The following findings were made. (1) Although AMs were generally found to release more inflammatory mediators than TII cells following LPS or silica exposure, primary TII cells clearly produced significant levels of mediators that could be capable of contributing considerably to lung inflammation and injury. (2) Since the responses of the RLE-6TN cell line to LPS or silica exposure were generally considerably less intense and required higher concentrations of stimulant than those measured in primary rat TII cells, RLE-6TN cells may not be an ideal substitute for primary TII cells in studying pulmonary inflammation. (3) LPS was more potent than silica in inducing inflammatory cytokine release from the three cell types. However, compared to LPS, silica exhibited equal or greater potency as an inducer of cellular oxidant generation, especially from primary TII cells.
Keywords
Laboratory-animals; Animals; Animal-studies; Silica-dusts; Silicates; Exposure-levels; Toxins; Toxic-effects; Pulmonary-system-disorders; Respiratory-system-disorders; Exposure-assessment; Lung-disorders
Contact
Vincent Castranova, PhD, NIOSH, 1095 Willowdale Road, M/S 2015, Morgantown, WV 26505, USA
CODEN
JTEHD6
CAS No.
14808-60-7
Publication Date
20050213
Document Type
Journal Article
Email Address
vic1@cdc.gov
Fiscal Year
2005
NTIS Accession No.
NTIS Price
Issue of Publication
3
ISSN
1528-7394
NIOSH Division
HELD
Source Name
Journal of Toxicology and Environmental Health, Part A: Current Issues
State
WV
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