Skip Navigation

This Article
Right arrow FREE Full Text (PDF) Freely available
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (10)
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Koike, E.
Right arrow Articles by Holt, P. G.
Right arrow Search for Related Content
PubMed
Right arrow Articles by Koike, E.
Right arrow Articles by Holt, P. G.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© 1998 Oxford University Press

research-article

Effect of Ozone Exposure on Alveolar Macrophage-Mediated Immunosuppressive Activity in Rats

Eiko Koike*, Takahiro Kobayashi{dagger},1, Delia J. Nelson{ddagger}, Andrew S. McWilliam{ddagger} and Patrick G. Holt{ddagger}

*Department of Medical Sciences, Tsukuba University Tsukuba 305, Japan {dagger}Environmental Health Sciences Division, National Institute for Environmental Studies Tsukuba 305, Japan {ddagger}TVW Telethon Institute for Child Health Research West Perth, Western Australia, Australia

Received June 20, 1997; accepted December 12, 1997

Effect of Ozone Exposure on Alveolar Macrophage-Mediated Immunosuppressive Activity in Rats, Koike, E., Kobayashi, T., Nelson, D.J., McWilliam, A.S., and Holt, P.G. (1998). ToxicoL Sci. 41, 217-223.

Ozone (O3), a major component of photochemical air pollution, is a strong oxidizing agent and highly toxic Resident alveolar macrophages (AM) play an important immunomodulatory role in the lung via suppression of lymphocyte proliferation, thus limiting the magnitude and duration of local immune responses. Nitric oxide (NO) plays a crucial role in the immunosuppressive activity of AM. However, during inununoinflammatory responses, microenvironmental changes within the alveoli inhibit this AM function, permitting full expression of local T-cell-mediated immune responses. We hypothesize that similar changes in AM function may occur during inflammation induced by exposure to inorganic air pollutants, such as O3. In order to test this hypothesis, in the present study, we investigated (1) whether O3 exposure of rats might affect the immunosuppressive activity and NO production of bronchoalveolar lavage cells (BAL cells) and (2) whether changes in the microenvironment of the alveoli induced by O3 exposure can affect the immunosuppressive activity and NO production of AM. AM-mediated immunosuppressive activity was measured as inhibition of concanavalin A (Con A>induced proliferation of lymph node cells (LNC). Bronchoalveolar lavage was used to sample the alveolar microenvironment, and the resulting fluid (BALF) was tested for capacity to modulate AM activity in the cultures. BALF and BAL cells from rats exposed to 1 ppm O3 or filtered air for 3 days were used. The present results demonstrate that BAL cells isolated from O3-exposed rats suppressed Con A-induced LNC proliferation and produced NO in the same manner as BAL cells (AM) from air-exposed rats. AM-mediated suppressive activity of LNC proliferation and NO production were markedly inhibited by BALF from 03-exposed but not from air-exposed rats. These results suggested that AM-mediated immunosuppressive activity in vivo may be inhibited by the O3-induced release of soluble factors which inhibit NO production by AM.


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 Toxicol SciHome page
E. Koike, T. Kobayashi, and N. Shimojo
Ozone Exposure Enhances Expression of Cell-Surface Molecules Associated with Antigen-Presenting Activity on Bronchoalveolar Lavage Cells in Rats
Toxicol. Sci., September 1, 2001; 63(1): 115 - 124.
[Abstract] [Full Text] [PDF]


Disclaimer:
Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.