title: Airborne Asian sand dust enhances murine lung eosinophilia.
abstract: There is no experimental study demonstrating the effects of airborne Asian sand dust (AASD) on allergic lung eosinophilia. The organic substances adsorbed onto AASD collected from the atmosphere of Iki-island in Japan were excluded by heat treatment at 360°C for 30 min. The effects of AASD or heated-AASD (H-AASD) towards allergic lung inflammation were compared in murine lungs to investigate the role of organic substances. ICR mice were administrated with the two kinds of AASD and/or ovalbumin (OVA) intratracheally four times at 2-week intervals. AASD and H-AASD 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. AASD and H-AASD synergistically increased Th2 cytokines-interleukin-13 (IL-13), eosinophil-relevant cytokine and chemokine, such as IL-5, and monocyte chemotactic protein-3 (MCP-3) induced by OVA in whole lung lavage fluid. The enhancing effects were much greater in AASD than in H-AASD. AASD induced adjuvant effects on OVA-specific immunoglobulin E (IgE) and IgG1 production. In an in vitro study using RAW264.7 cells, AASD increased the expression of Toll-like receptors 2 (TLR2) mRNA, but not TLR4 mRNA. AASD increased mRNA expression of NALP3, ASC, and IL-1ß compared with the control. H-AASD caused no expression of either mRNA. These results suggest that the aggravated lung eosinophilia in AASD is due to activation of a Th2-associated immune response and that the activation of TLR2 and NALP3 inflammasome by microbial materials could be participating in this phenomenon.
authors.affiliation: Department of Environmental and Occupational Health, College of Public Health, China Medical University, Shenyang, China.
authors.forename: Miao
authors.initials: M
authors.lastname: He
authors.forename: Takamichi
authors.initials: T
authors.lastname: Ichinose
authors.forename: Seiichi
authors.initials: S
authors.lastname: Yoshida
authors.forename: Masataka
authors.initials: M
authors.lastname: Nishikawa
authors.forename: Ikuko
authors.initials: I
authors.lastname: Mori
authors.forename: Rie
authors.initials: R
authors.lastname: Yanagisawa
authors.forename: Hirohisa
authors.initials: H
authors.lastname: Takano
authors.forename: Ken-ichiro
authors.initials: K
authors.lastname: Inoue
authors.forename: Guifan
authors.initials: G
authors.lastname: Sun
authors.forename: Takayuki
authors.initials: T
authors.lastname: Shibamoto
mesh_terms: D000393:Air Pollutants / Q000276:immunology / Q000633:toxicity*; D000397:Air Pollution; D000818:Animals; D002352:Carrier Proteins / Q000235:genetics / Q000378:metabolism; D002460:Cell Line; D016207:Cytokines / Q000378:metabolism; D004357:Drug Synergism; D004391:Dust / Q000276:immunology; D004804:Eosinophils / Q000187:drug effects* / Q000276:immunology / Q000473:pathology; D015870:Gene Expression / Q000187:drug effects; D007136:Immunoglobulins / Q000378:metabolism; D019570:Inhalation Exposure; D008264:Macrophages / Q000187:drug effects / Q000276:immunology / Q000473:pathology; D008297:Male; D051379:Mice; D008813:Mice, Inbred ICR; D000071199:NLR Family, Pyrin Domain-Containing 3 Protein; D010047:Ovalbumin / Q000276:immunology; D052638:Particulate Matter; D011650:Pulmonary Alveoli / Q000187:drug effects / Q000276:immunology / Q000473:pathology; D011657:Pulmonary Eosinophilia / Q000139:chemically induced* / Q000276:immunology / Q000473:pathology; D012822:Silicon Dioxide / Q000276:immunology / Q000633:toxicity*; D051195:Toll-Like Receptor 2 / Q000235:genetics / Q000378:metabolism
chemical_list: D000393:Air Pollutants; D002352:Carrier Proteins; D016207:Cytokines; D004391:Dust; D007136:Immunoglobulins; D000071199:NLR Family, Pyrin Domain-Containing 3 Protein; C492716:Nlrp3 protein, mouse; D052638:Particulate Matter; C493486:Tlr2 protein, mouse; D051195:Toll-Like Receptor 2; D012822:Silicon Dioxide; D010047:Ovalbumin