title: Enhancement of OVA-induced murine lung eosinophilia by co-exposure to contamination levels of LPS in Asian sand dust and heated dust.
abstract: BACKGROUND
  A previous study has shown that the aggravation of Asian sand dust (ASD) on ovalbumin (OVA)-induced lung eosinphilia was more severe in lipopolysaccharide (LPS)-rich ASD than in SiO2-rich ASD. Therefore, the effects of different LPS contamination levels in ASD on the aggravation of OVA-induced lung eosinophilia were investigated in the present study.
  
  
  METHODS
  Before beginning the in vivo experiment, we investigated whether the ultra-pure LPS would act only on TLR4 or not using bone marrow-derived macrophages (BMDMs) of wild-type, TLR2-/-, TLR4-/- and MyD88-/- BALB/c mice. ASD collected from the desert was heated to remove toxic organic substances (H-ASD). BALB/c mice were instilled intratracheally with 12 different testing samples prepared with LPS (1 ng and 10 ng), H-ASD, and OVA in a normal saline solution. The lung pathology, cytological profiles in the bronchoalveolar lavage fluid (BALF), the levels of inflammatory cytokines/chemokines in BALF and OVA-specific immunoglobulin in serum were investigated.
  
  
  RESULTS
  The LPS exhibited no response to the production of TNF-α and IL-6 in BMDMs from TLR4-/-, but did from TLR2-/-. H-ASD aggravated the LPS-induced neutrophilic lung inflammation. In the presence of OVA, LPS increased the level of eosinophils slightly and induced trace levels of Th2 cytokines IL-5 and IL-13 at the levels of 1 ng and 10 ng. In the presence of OVA and H-ASD, LPS induced severe eosinophil infiltration and proliferation of goblet cells in the airways as well as remarkable increases in Th2 cytokines IL-5 and IL-13 in BALF. The mixture containing LPS (1 ng) showed adjuvant activity on OVA-specific IgE and IgG1 production.
  
  
  CONCLUSIONS
  The results suggest that H-ASD with naturally-occurring levels of LPS enhances OVA-induced lung eosinophilia via increases in Th2-mediated cytokines and antigen-specific immunoglobulin. These results indicate that LPS is a strong candidate for being a major aggravating substance in ASD.
authors: Department of Nutritional and Food Hygiene, College of Public Health, China Medical University, Shenyang, China.
authors: Yahao
authors: Y
authors: Ren
authors: Department of Health Sciences, Oita University of Nursing and Health Sciences, Oita 870-1201, Japan.
authors: Takamichi
authors: T
authors: Ichinose
authors: Department of Environmental and Occupational Health, College of Public Health, China Medical University, Shenyang, China.
authors: Miao
authors: M
authors: He
authors: Department of Immunology and Parasitology, School of Medicine, University of Occupational and Environmental Health, Japan, Fukuoka 807-8555, Japan.
authors: Yuan
authors: Y
authors: Song
authors: Department of Immunology and Parasitology, School of Medicine, University of Occupational and Environmental Health, Japan, Fukuoka 807-8555, Japan.
authors: Yasuhiro
authors: Y
authors: Yoshida
authors: Department of Health Sciences, Oita University of Nursing and Health Sciences, Oita 870-1201, Japan.
authors: Seiichi
authors: S
authors: Yoshida
authors: Environmental Chemistry Division, National Institute for Environmental Studies, Ibaraki 305-8506, Japan.
authors: Masataka
authors: M
authors: Nishikawa
authors: Environmental Health Division, Department of Environmental Engineering, Graduate School of Engineering, Kyoto University, Kyoto 615-8530, Japan.
authors: Hirohisa
authors: H
authors: Takano
authors: Department of Environmental and Occupational Health, College of Public Health, China Medical University, Shenyang, China.
authors: Guifan
authors: G
authors: Sun
authors: Department of Environmental Toxicology, University of California, Davis, CA 95616, USA.
authors: Takayuki
authors: T
authors: Shibamoto
keywords: Asian sand dust; Asthma; Cytokine and chemokine; Lipopolysaccharide; Lung eosinophilia; Ovalbumin