PMID- 20849355 OWN - NLM STAT- MEDLINE DCOM- 20110111 LR - 20161125 IS - 1091-7691 (Electronic) IS - 0895-8378 (Linking) VI - 22 IP - 12 DP - 2010 Oct TI - Airborne Asian sand dust enhances murine lung eosinophilia. PG - 1012-25 LID - 10.3109/08958378.2010.510151 [doi] AB - 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 degrees 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. FAU - He, Miao AU - He M AD - Department of Environmental and Occupational Health, College of Public Health, China Medical University, Shenyang, China. FAU - Ichinose, Takamichi AU - Ichinose T FAU - Yoshida, Seiichi AU - Yoshida S FAU - Nishikawa, Masataka AU - Nishikawa M FAU - Mori, Ikuko AU - Mori I FAU - Yanagisawa, Rie AU - Yanagisawa R FAU - Takano, Hirohisa AU - Takano H FAU - Inoue, Ken-ichiro AU - Inoue K FAU - Sun, Guifan AU - Sun G FAU - Shibamoto, Takayuki AU - Shibamoto T LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't PL - England TA - Inhal Toxicol JT - Inhalation toxicology JID - 8910739 RN - 0 (Air Pollutants) RN - 0 (Carrier Proteins) RN - 0 (Cytokines) RN - 0 (Dust) RN - 0 (Immunoglobulins) RN - 0 (NLR Family, Pyrin Domain-Containing 3 Protein) RN - 0 (Nlrp3 protein, mouse) RN - 0 (Particulate Matter) RN - 0 (Tlr2 protein, mouse) RN - 0 (Toll-Like Receptor 2) RN - 7631-86-9 (Silicon Dioxide) RN - 9006-59-1 (Ovalbumin) SB - IM MH - Air Pollutants/immunology/*toxicity MH - *Air Pollution MH - Animals MH - Carrier Proteins/genetics/metabolism MH - Cell Line MH - Cytokines/metabolism MH - Drug Synergism MH - Dust/immunology MH - Eosinophils/*drug effects/immunology/pathology MH - Gene Expression/drug effects MH - Immunoglobulins/metabolism MH - Inhalation Exposure MH - Macrophages/drug effects/immunology/pathology MH - Male MH - Mice MH - Mice, Inbred ICR MH - NLR Family, Pyrin Domain-Containing 3 Protein MH - Ovalbumin/immunology MH - Particulate Matter MH - Pulmonary Alveoli/drug effects/immunology/pathology MH - Pulmonary Eosinophilia/*chemically induced/immunology/pathology MH - Silicon Dioxide/immunology/*toxicity MH - Toll-Like Receptor 2/genetics/metabolism EDAT- 2010/09/21 06:00 MHDA- 2011/01/12 06:00 CRDT- 2010/09/21 06:00 PHST- 2010/09/21 06:00 [entrez] PHST- 2010/09/21 06:00 [pubmed] PHST- 2011/01/12 06:00 [medline] AID - 10.3109/08958378.2010.510151 [doi] PST - ppublish SO - Inhal Toxicol. 2010 Oct;22(12):1012-25. doi: 10.3109/08958378.2010.510151.