title: Aggravation of ovalbumin-induced murine asthma by co-exposure to desert-dust and organic chemicals: an animal model study.
abstract: BACKGROUND
  The organic chemicals present in Asian sand dust (ASD) might contribute to the aggravation of lung eosinophila. Therefore, the aggravating effects of the Tar fraction from ASD on ovalbumin (OVA)-induced lung eosinophilia were investigated.
  
  
  METHODS
  The Tar fraction was extracted from ASD collected from the atmosphere in Fukuoka, Japan. ASD collected from the Gobi desert was heated at 360°C to inactivate toxic organic substances (H-ASD). ICR mice were instilled intratracheally with 12 different test samples prepared with Tar (1 μg and 5 μg), H-ASD, and OVA in a normal saline solution containing 0.02% Tween 80. The lung pathology, cytological profiles in the bronchoalveolar lavage fluid (BALF), inflammatory cytokines/chemokines in BALF and OVA-specific immunoglobulin in serum were investigated.
  
  
  RESULTS
  Several kinds of polycyclic aromatic hydrocarbons (PAHs) were detected in the Tar sample. H-ASD + Tar 5 μg induced slight neutrophilic lung inflammation. In the presence of OVA, Tar 5 μg increased the level of eosinophils slightly and induced trace levels of Th2 cytokines IL-5 and IL-13 in BALF. Also mild to moderate goblet cell proliferation and mild infiltration of eosinophils in the submucosa of airway were observed. These pathological changes caused by H-ASD + OVA were relatively small. However, in the presence of OVA and H-ASD, Tar, at as low a level as 1 μg, induced severe eosinophil infiltration and proliferation of goblet cells in the airways and significantly increased Th2 cytokines IL-5 and IL-13 in BALF. The mixture showed an adjuvant effect on OVA-specific IgG1 production.
  
  
  CONCLUSIONS
  These results indicate that H-ASD with even low levels of Tar exacerbates OVA-induced lung eosinophilia via increases of Th2-mediated cytokines. These results suggest that ASD-bound PAHs might contribute to the aggravation of lung eosinophila.
authors.forename: Yahao
authors.initials: Y
authors.lastname: Ren
authors.affiliation: Department of Health Sciences, Oita University of Nursing and Health Sciences, Oita, Japan. ichinose@oita-nhs.ac.jp.
authors.forename: Takamichi
authors.initials: T
authors.lastname: Ichinose
authors.forename: Miao
authors.initials: M
authors.lastname: He
authors.forename: Keiichi
authors.initials: K
authors.lastname: Arashidani
authors.forename: Yasuhiro
authors.initials: Y
authors.lastname: Yoshida
authors.forename: Seiichi
authors.initials: S
authors.lastname: Yoshida
authors.forename: Masataka
authors.initials: M
authors.lastname: Nishikawa
authors.forename: Hirohisa
authors.initials: H
authors.lastname: Takano
authors.forename: Guifan
authors.initials: G
authors.lastname: Sun
authors.forename: Takayuki
authors.initials: T
authors.lastname: Shibamoto
mesh_terms: D000393:Air Pollutants / Q000633:toxicity*; D000818:Animals; D001249:Asthma / Q000139:chemically induced / Q000473:pathology; D004195:Disease Models, Animal; D004391:Dust / Q000032:analysis*; D008168:Lung / Q000187:drug effects* / Q000473:pathology / Q000503:physiopathology; D008297:Male; D051379:Mice; D008813:Mice, Inbred ICR; D010047:Ovalbumin / Q000633:toxicity; D011657:Pulmonary Eosinophilia / Q000139:chemically induced / Q000473:pathology* / Q000503:physiopathology*; D013047:Specific Pathogen-Free Organisms; D013638:Tars / Q000633:toxicity*
chemical_list: D000393:Air Pollutants; D004391:Dust; D013638:Tars; D010047:Ovalbumin