PMID- 20560731 OWN - NLM STAT- MEDLINE DCOM- 20101019 LR - 20100719 IS - 1091-7691 (Electronic) IS - 0895-8378 (Linking) VI - 22 IP - 9 DP - 2010 Aug TI - Urban particulate matter in Beijing, China, enhances allergen-induced murine lung eosinophilia. PG - 709-18 LID - 10.3109/08958371003631608 [doi] AB - It has been reported that ambient particulate matter (PM) in some large cities, such as Beijing, China, causes adverse respiratory health effects. However, there is currently no experimental report on the relationship between bronchial asthma and urban PM (UPM) in northeast Asia. In this study, the microbial and chemical substances adsorbed onto UPM collected in Beijing were excluded by heat-treatment at 360 degrees C for 30 min. The effects of UPM or heated UPM (H-UPM) toward allergic lung inflammation were compared in murine lungs to investigate the role of organic substances. ICR mice were administrated intratracheally with the two kinds of UPM and/or ovalbumin (OVA) 4 times at 2-week intervals. UPM and H-UPM 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. UPM and H-UPM synergistically increased Th-2 cytokines--interleukin (IL)-4 and IL-13, eosinophil-relevant cytokines and chemokines, such as IL-5 and monocyte chemotactic protein-3 (MCP-3), induced by OVA in bronchoalveolar lavage fluid (BALF). The enhancing effects were much greater in UPM than in H-UPM. UPM induced adjuvant effects on specific immunoglobulin E (IgE) and IgG1 production by OVA. In an in vitro study using RAW264.7 cells, UPM increased the expression of Toll-like receptor 2 (TLR2) mRNA, but not TLR4 mRNA. H-UPM caused no expression of both TLR mRNAs. These results suggest that the aggravated lung eosinophilia in UPM was due to activation of a Th2-associated immune response via the activation of TLR2 by microbial materials. Chemical materials of air pollutant origin contained in UPM, and inorganic components (elemental carbon, mineral elements) in H-UPM, could also cause the aggravation. 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 (Chemokines) RN - 0 (Particulate Matter) RN - 0 (RNA, Messenger) RN - 0 (Tlr2 protein, mouse) RN - 0 (Tlr4 protein, mouse) RN - 0 (Toll-Like Receptor 2) RN - 0 (Toll-Like Receptor 4) RN - 9006-59-1 (Ovalbumin) SB - IM MH - Air Pollutants/*toxicity MH - Animals MH - Bronchoalveolar Lavage Fluid/chemistry/cytology MH - Cell Line MH - Chemokines/metabolism MH - China MH - Drug Synergism MH - Eosinophils/*drug effects/pathology MH - Gene Expression/drug effects MH - Hot Temperature MH - Intubation, Intratracheal MH - Lung/*drug effects/immunology/pathology MH - Macrophages/drug effects/metabolism/pathology MH - Male MH - Mice MH - Mice, Inbred BALB C MH - Mice, Inbred ICR MH - Ovalbumin/administration & dosage/immunology MH - Particulate Matter/*toxicity MH - Pulmonary Alveoli/drug effects/metabolism/pathology MH - Pulmonary Eosinophilia/*chemically induced/immunology/pathology MH - RNA, Messenger/metabolism MH - Toll-Like Receptor 2/genetics/metabolism MH - Toll-Like Receptor 4/genetics/metabolism EDAT- 2010/06/22 06:00 MHDA- 2010/10/20 06:00 CRDT- 2010/06/22 06:00 PHST- 2010/06/22 06:00 [entrez] PHST- 2010/06/22 06:00 [pubmed] PHST- 2010/10/20 06:00 [medline] AID - 10.3109/08958371003631608 [doi] PST - ppublish SO - Inhal Toxicol. 2010 Aug;22(9):709-18. doi: 10.3109/08958371003631608.