Skip directly to search Skip directly to A to Z list Skip directly to page options Skip directly to site content

NIOSHTIC-2 Publications Search

Search Results

Dual acute proinflammatory and antifibrotic pulmonary effects of short palate, lung, and nasal epithelium clone-1 after exposure to carbon nanotubes.

Authors
Di-YP; Tkach-AV; Yanamala-N; Stanley-S; Gao-SL; Shurin-MR; Kisin-ER; Kagan-VE; Shvedova-A
Source
Am J Respir Cell Mol Biol 2013 Nov; 49(5):759-767
NIOSHTIC No.
20043566
Abstract
Carbon nanotubes (CNTs; allotropes of carbon with a cylindrical nanostructure) have emerged as one of the most commonly used types of nanomaterials, with numerous applications in industry and biomedicine. However, the inhalation of CNTs has been shown to elicit pulmonary toxicity, accompanied by a robust inflammatory response with an early-onset fibrotic phase. Epithelial host-defense proteins represent an important component of the pulmonary innate immune response to foreign inhalants such as particles and bacteria. The short palate, lung, and nasal epithelium clone-1 (SPLUNC1) protein, a member of the bactericidal/permeability-increasing-fold (BPIF)-containing protein family, is a 25-kD secretory protein that is expressed in nasal, oropharyngeal, and lung epithelia, and has been shown to have multiple functions, including antimicrobial and chemotactic activities, as well as surfactant properties. This study sought to assess the importance of SPLUNC1-mediated pulmonary responses in airway epithelial secretions, and to explore the biological relevance of SPLUNC1 to inhaled particles in a single-walled carbon nanotube (SWCNT) model. Using Scgb1a1-hSPLUNC1 transgenic mice, we observed that SPLUNC1 significantly modified host inflammatory responses by increasing leukocyte recruitment and enhancing phagocytic activity. Furthermore, we found that transgenic mice were more susceptible to SWCNT exposure at the acute phase, but showed resistance against lung fibrogenesis through pathological changes in the long term. The binding of SPLUNC1 also attenuated SWCNT-induced TNF-alpha secretion by RAW 264.7 macrophages. Taken together, our data indicate that SPLUNC1 is an important component of mucosal innate immune defense against pulmonary inhaled particles.
Keywords
Nanotechnology; Respiratory-system-disorders; Immune-reaction; Fibrous-bodies; Host-resistance; Proteins; Glycoproteins; Pulmonary-system-disorders; Lung-cells; Lung-disorders; Lung-fibrosis; Inhalants; Bactericides; Antibacterial-agents; Surfactants; Airway-resistance; Animal-studies; Animals; Laboratory-animals; Laboratory-testing; Phagocytes; Leukocytes; Exposure-assessment; Fibrogenesis; Mucous-membranes; Metabolism; Immunology; Pathology; Alveolar-cells; Author Keywords: SPLUNC1; BPIFA1; carbon nanotube; fibrosis; inflammation
Contact
Y. Peter Di, Ph.D., Department of Environmental and Occupational Health, University of Pittsburgh, 100 Technology Drive, Suite 322, Bridgeside Point, Pittsburgh, PA 15219
CODEN
AJRBEL
CAS No.
7440-44-0
Publication Date
20131101
Document Type
Journal Article
Email Address
peterdi@pitt.edu; ats1@cdc.gov
Fiscal Year
2014
NTIS Accession No.
NTIS Price
Issue of Publication
5
ISSN
1044-1549
NIOSH Division
HELD
Priority Area
Manufacturing
Source Name
American Journal of Respiratory Cell and Molecular Biology
State
PA; WV
TOP