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Lung macrophage-epithelial cell interactions amplify particle-mediated cytokine release
1Department of Environmental Health, Harvard School of Public Health, Boston, Massachusetts 02115, USA. ftao@hpsh.harvard.edu
American Journal of Respiratory Cell and Molecular Biology
|March 29, 2002
Summary
Air pollution particles trigger inflammatory responses through interactions between alveolar macrophages (AMs) and epithelial cells. This contact-dependent potentiation enhances cytokine release, suggesting a novel in vitro model for particle effects.
Area of Science:
- Pulmonary toxicology
- Cellular immunology
- Environmental health
Background:
- Alveolar macrophages (AMs) and epithelial cells interact during inflammatory responses.
- Air pollution particles are known to elicit inflammatory reactions in the lungs.
Purpose of the Study:
- To investigate the role of AM-epithelial cell interactions in inflammatory responses to air pollution particles.
- To determine if co-culture enhances particle-induced cytokine release.
Main Methods:
- Rat AMs and RLE-6TN epithelial cells were cultured alone or co-cultured.
- Cells were exposed to titanium dioxide, alpha-quartz, ROFA, or UAP (0-50 microg/ml) for 24 hours.
- Tumor necrosis factor-alpha (TNF-alpha) and macrophage inflammatory protein-2 (MIP-2) release were measured.
Main Results:
- Co-culture of AMs and RLE cells synergistically increased basal and particle-induced TNF-alpha and MIP-2 release compared to monocultures.
- This potentiation was contact-dependent and not observed with fibroblasts.
- Cytokine release was not enhanced when AMs and RLE cells were physically separated.
Conclusions:
- Contact-dependent interactions between AMs and epithelial cells amplify inflammatory responses to particles.
- AM-epithelial co-culture serves as a valuable in vitro model for studying in vivo particle effects.