help button home button Am J Pathol sign up for etoc
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS

This Article
Right arrow Order Full text via Infotrieve
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Absher, M. P.
Right arrow Articles by Leslie, K. O.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Absher, M. P.
Right arrow Articles by Leslie, K. O.

American Journal of Pathology, Vol 134, 1243-1251, Copyright © 1989 by American Society for Investigative Pathology


REGULAR ARTICLES

Biphasic cellular and tissue response of rat lungs after eight-day aerosol exposure to the silicon dioxide cristobalite

MP Absher, L Trombley, DR Hemenway, RM Mickey and KO Leslie
Department of Medicine, University of Vermont, Burlington.

Cristobalite is a crystalline silicon dioxide that elicits pulmonary inflammation and fibrosis in humans and experimental animals. Exposure of rats to aerosols of respirable cristobalite for 8 days led to a rapid influx of neutrophils and macrophages into alveolar and tissue compartments of the lung followed by a more gradual accumulation of T lymphocytes. This inflammatory response persisted throughout 52 weeks after the end of the exposure. For some variables studied there appeared to be a cyclical nature to the response. Statistical analysis of alveolar cell populations and lung tissue weight, protein, and hydroxyproline showed significant time-dependent fluctuations. Histologic analysis revealed a progressive deposition of collagen and type II cell hyperplasia centered on airways, however, there appeared to be some correlation between fluctuations in alveolar cell populations and overall tissue pathology. The observed cellular and biochemical fluctuations and the persistence of the inflammatory response may be due to the presence of silica in the lung, which serves as a source of repetitive stimulation of lung cells.


This article has been cited by other articles:


Home page
Toxicol SciHome page
S.-H. Huang, A. F. Hubbs, C. F. Stanley, V. Vallyathan, P. C. Schnabel, Y. Rojanasakul, J. K. H. Ma, D. E. Banks, and D. N. Weissman
Immunoglobulin Responses to Experimental Silicosis
Toxicol. Sci., January 1, 2001; 59(1): 108 - 117.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Respir. Cell Mol. Bio.Home page
G. S. Davis, L. M. Pfeiffer, and D. R. Hemenway
Interferon-gamma Production by Specific Lung Lymphocyte Phenotypes in Silicosis in Mice
Am. J. Respir. Cell Mol. Biol., April 1, 2000; 22(4): 491 - 501.
[Abstract] [Full Text]


Home page
Am. J. Respir. Cell Mol. Bio.Home page
G. S. Davis, L. M. Pfeiffer, and D. R. Hemenway
Expansion of Interferon-gamma -Producing Lung Lymphocytes in Mouse Silicosis
Am. J. Respir. Cell Mol. Biol., April 1, 1999; 20(4): 813 - 824.
[Abstract] [Full Text]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1989 by the American Society for Investigative Pathology.