title: The effects of microbial materials adhered to Asian sand dust on allergic lung inflammation.
abstract: Asian sand dust (ASD) containing microbiological materials, sulfate (SO(4)(2)), and nitrate (NO(3)(-) ) derived from air pollutants in East China, reportedly cause adverse respiratory health effects. ASD aggravates ovalbumin (OVA)-associated experimental lung eosinophilia. In this study, the toxic materials adsorbed onto ASD were excluded by heat treatment at 360 degrees C for 30 min. The effects of nonheated ASD or heated ASD (H-ASD) toward the allergic lung inflammation were compared in murine lungs. ICR mice were administered intratracheally with normal saline (control), H-ASD, ASD, OVA, OVA + H-ASD, and OVA + ASD, four times at 2-week intervals. ASD only increased neutrophils in bronchoalveolar lavage fluids (BALFs) along with pro-inflammatory mediators, such as keratinocyte chemoattractant (KC). H-ASD and ASD enhanced eosinophil recruitment induced by OVA in the alveoli and in the submucosa of the airway, which has a goblet cell proliferation in the bronchial epithelium. The two ASDs synergistically increased interleukin-5 (IL-5), monocyte chemotactic protein-3 (MCP-3), and eotaxin, which were associated with OVA, in BALF. The enhancing effects were much greater in ASD than in H-ASD. The two ASDs induced the adjuvant effects to specific IgE and IgG1 production by OVA. In the in vitro study using RAW264.7 cells, ASD increased the expression of Toll-like receptor 2 (TLR 2) mRNA but not TLR4 mRNA. H-ASD caused no expression of either TLR mRNA. These results suggest that the aggravated lung eosinophilia by ASD may be due to activation of Th2-associated immune response via the activation of TLR2 by microbial components adhered to ASD.
authors.affiliation: Department of Health Sciences, Oita University of Nursing and Health Sciences, Notsuharu, Oita, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Ichinose
authors.forename: S
authors.initials: S
authors.lastname: Yoshida
authors.forename: K
authors.initials: K
authors.lastname: Hiyoshi
authors.forename: K
authors.initials: K
authors.lastname: Sadakane
authors.forename: H
authors.initials: H
authors.lastname: Takano
authors.forename: M
authors.initials: M
authors.lastname: Nishikawa
authors.forename: I
authors.initials: I
authors.lastname: Mori
authors.forename: R
authors.initials: R
authors.lastname: Yanagisawa
authors.forename: H
authors.initials: H
authors.lastname: Kawazato
authors.forename: A
authors.initials: A
authors.lastname: Yasuda
authors.forename: T
authors.initials: T
authors.lastname: Shibamoto
mesh_terms: D000391:Air Microbiology / Q000592:standards*; D000393:Air Pollutants / Q000633:toxicity*; D000818:Animals; D018893:Bronchoalveolar Lavage; D001992:Bronchoalveolar Lavage Fluid; D004190:Disasters; D004195:Disease Models, Animal; D004391:Dust / Q000032:analysis*; D008168:Lung / Q000187:drug effects / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D008297:Male; D051379:Mice; D008813:Mice, Inbred ICR; D010316:Particle Size; D011014:Pneumonia / Q000209:etiology* / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D012130:Respiratory Hypersensitivity / Q000209:etiology* / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D012822:Silicon Dioxide / Q000032:analysis*
chemical_list: D000393:Air Pollutants; D004391:Dust; D012822:Silicon Dioxide