title: Repeated pulmonary exposure to single-walled carbon nanotubes exacerbates allergic inflammation of the airway: Possible role of oxidative stress.
abstract: The development of nanotechnology has increased the risk of environmental exposure to types of particles other than those derived from combustion, namely, industrial nanomaterials. Patients with bronchial asthma are sensitive to inhaled substances, including particulate matter. This study examined the effects of pulmonary exposure to a type of nano-sized carbon nanotube (single-walled nanotubes (SWCNT)) on allergic airway inflammation and sought their cellular mechanisms. In the in vivo experiments, ICR mice were divided into four experimental groups that were repeatedly administered vehicle, SWCNT (50 microg/animal), ovalbumin (OVA; an allergen), or OVA + SWCNT through an intratracheal route and thereafter assayed. SWCNT aggravated allergen-induced pulmonary inflammation with mucus hyperplasia. SWCNT with allergen amplified lung protein levels of T helper (Th) cytokines and chemokines related to allergy and exhibited adjuvant activity for allergen-specific IgG(1) (and IgE) compared with allergen alone. SWCNT accentuated the level/activity of oxidative stress-related biomarkers in the airways in the presence of allergen. In vitro, SWCNT can partially promote/strengthen the maturation/activation/function of bone marrow-derived dendritic cells (DC). Together, these results suggest that SWCNT can exacerbate murine allergic airway inflammation via enhanced activation of Th immunity and increased oxidative stress. In addition, this exacerbation may be partly through the inappropriate activation of antigen-presenting cells, including DC.
authors.affiliation: National Institute for Environmental Studies, Tsukuba, Ibaraki, Japan. inoue.kenichirou@nies.go.jp
authors.forename: Ken-Ichiro
authors.initials: K
authors.lastname: Inoue
authors.forename: Rie
authors.initials: R
authors.lastname: Yanagisawa
authors.forename: Eiko
authors.initials: E
authors.lastname: Koike
authors.forename: Masataka
authors.initials: M
authors.lastname: Nishikawa
authors.forename: Hirohisa
authors.initials: H
authors.lastname: Takano
mesh_terms: D000485:Allergens / Q000276:immunology; D000818:Animals; D001249:Asthma / Q000378:metabolism* / Q000503:physiopathology; D016535:Bronchial Hyperreactivity; D016207:Cytokines / Q000378:metabolism; D018450:Disease Progression; D004781:Environmental Exposure / Q000009:adverse effects*; D006965:Hyperplasia; D007111:Immunity, Cellular; D007073:Immunoglobulin E / Q000097:blood; D007074:Immunoglobulin G / Q000097:blood; D007249:Inflammation; D008168:Lung / Q000473:pathology; D008297:Male; D051379:Mice; D008813:Mice, Inbred ICR; D037742:Nanotubes, Carbon / Q000009:adverse effects*; D010047:Ovalbumin / Q000276:immunology; D018384:Oxidative Stress; D020545:Respiratory Mucosa
chemical_list: D000485:Allergens; D016207:Cytokines; D007074:Immunoglobulin G; D037742:Nanotubes, Carbon; D007073:Immunoglobulin E; D010047:Ovalbumin