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Am J Physiol Lung Cell Mol Physiol 289: L698-L708, 2005. First published June 10, 2005; doi:10.1152/ajplung.00084.2005
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EDITORIAL FOCUS

Unusual inflammatory and fibrogenic pulmonary responses to single-walled carbon nanotubes in mice

Anna A. Shvedova,1 Elena R. Kisin,1 Robert Mercer,1 Ashley R. Murray,1 Victor J. Johnson,1 Alla I. Potapovich,4,5 Yulia Y. Tyurina,4,5 Olga Gorelik,3 Sevaram Arepalli,3 Diane Schwegler-Berry,1 Ann F. Hubbs,1 James Antonini,1 Douglas E. Evans,2 Bon-Ki Ku,2 Dawn Ramsey,2 Andrew Maynard,2 Valerian E. Kagan,4,5 Vincent Castranova,1,5 and Paul Baron2

1Health Effects Laboratory Division, National Institute for Occupational Safety and Health, Morgantown, West Virginia; 2Division of Applied Research and Technology, National Institute for Occupational Safety and Health, Cincinnati, Ohio; 3Nanotube Team, GBTech, Incorporated, National Aeronautics and Space Administration-Johnson Space Center, Houston, Texas; and 4Center for Free Radical & Antioxidant Health and 5Department of Environmental Health, University of Pittsburgh, Pittsburgh, Pennsylvania

Submitted 22 February 2005 ; accepted in final form 7 June 2005

Single-walled carbon nanotubes (SWCNT) are new materials of emerging technological importance. As SWCNT are introduced into the life cycle of commercial products, their effects on human health and environment should be addressed. We demonstrated that pharyngeal aspiration of SWCNT elicited unusual pulmonary effects in C57BL/6 mice that combined a robust but acute inflammation with early onset yet progressive fibrosis and granulomas. A dose-dependent increase in the protein, LDH, and {gamma}-glutamyl transferase activities in bronchoalveolar lavage were found along with accumulation of 4-hydroxynonenal (oxidative biomarker) and depletion of glutathione in lungs. An early neutrophils accumulation (day 1), followed by lymphocyte (day 3) and macrophage (day 7) influx, was accompanied by early elevation of proinflammatory cytokines (TNF-{alpha}, IL-1{beta}; day 1) followed by fibrogenic transforming growth factor (TGF)-{beta}1 (peaked on day 7). A rapid progressive fibrosis found in mice exhibited two distinct morphologies: 1) SWCNT-induced granulomas mainly associated with hypertrophied epithelial cells surrounding SWCNT aggregates and 2) diffuse interstitial fibrosis and alveolar wall thickening likely associated with dispersed SWCNT. In vitro exposure of murine RAW 264.7 macrophages to SWCNT triggered TGF-{beta}1 production similarly to zymosan but generated less TNF-{alpha} and IL-1{beta}. SWCNT did not cause superoxide or NO·production, active SWCNT engulfment, or apoptosis in RAW 264.7 macrophages. Functional respiratory deficiencies and decreased bacterial clearance (Listeria monocytogenes) were found in mice treated with SWCNT. Equal doses of ultrafine carbon black particles or fine crystalline silica (SiO2) did not induce granulomas or alveolar wall thickening and caused a significantly weaker pulmonary inflammation and damage.

nanoparticles; inflammation; cytokines; microbial infection


Address for reprint requests and other correspondence: A. A. Shvedova, Health Effects Laboratory Div., NIOSH, Morgantown, WV (e-mail: AShvedova{at}cdc.gov)




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