HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (9) Citing Articles via Google Scholar Google Scholar Articles by André, E. Articles by Wjst, M. Search for Related Content PubMed PubMed Citation Articles by André, E. Articles by Wjst, M.

Inhalation of ultrafine carbon particles triggers biphasic pro-inflammatory response in the mouse lung

¹ Ludwig-Maximilians-University, Institute for Epidemiology, ² GSF-National Research Center for Environment and Health, Institute for Epidemiology, and ³ GSF-National Research Center for Environment and Health, Institute for Inhalation Biology, Neuherberg, Germany. ⁴ Both authors contributed equally to this study.

CORRESPONDENCE: T. Stoeger, GSF-National Research Center for Environment and Health, Institute for Inhalation Biology, Ingolstaedter Landstrasse 1, D-85758 Neuherberg/Munich, Germany. Fax: 49 8931872400. E-mail: tobias.stoeger{at}gsf.de

Keywords: Air pollution, alveolar macrophages, cytokines, expression profiling

Received: June 16, 2005
Accepted April 20, 2006

High levels of particulate matter in ambient air are associated with increased respiratory and cardiovascular health problems. It has been hypothesised that it is the ultrafine particle fraction (diameter <100 nm) that is largely responsible for these effects. To evaluate the associated mechanisms on a molecular level, the current authors applied an expression profiling approach.

Healthy mice were exposed to either ultrafine carbon particles (UFCPs; mass concentration 380 µg·m^-3) or filtered air for 4 and 24 h. Histology of the lungs did not indicate any pathomorphological changes after inhalation.

Examination of the bronchoalveolar lavage fluid revealed a small increase in polymorphonuclear cell number (ranging 0.6–1%) after UFCP inhalation, compared with clean air controls, suggesting a minor inflammatory response. However, DNA microarray profile analysis revealed a clearly biphasic response to particle exposure. After 4 h of inhalation, mainly heat shock proteins were induced, whereas after 24 h, different immunomodulatory proteins (osteopontin, galectin-3 and lipocalin-2) were upregulated in alveolar macrophages and septal cells.

In conclusion, these data indicate that inhalation of ultrafine carbon particles triggers a biphasic pro-inflammatory process in the lung, involving the activation of macrophages and the upregulation of immunomodulatory proteins.

This article has been cited by other articles:

				J. W. Card, D. C. Zeldin, J. C. Bonner, and E. R. Nestmann Pulmonary applications and toxicity of engineered nanoparticles Am J Physiol Lung Cell Mol Physiol, September 1, 2008; 295(3): L400 - L411. [Abstract] [Full Text] [PDF]

				R. L. Rouse, G. Murphy, M. J. Boudreaux, D. B. Paulsen, and A. L. Penn Soot Nanoparticles Promote Biotransformation, Oxidative Stress, and Inflammation in Murine Lungs Am. J. Respir. Cell Mol. Biol., August 1, 2008; 39(2): 198 - 207. [Abstract] [Full Text] [PDF]