Urban particulate matter in Beijing, China, enhances allergen-induced murine lung eosinophilia.
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.
He
Miao
M
Department of Environmental and Occupational Health, College of Public Health, China Medical University, Shenyang, China.
Ichinose
Takamichi
T
Yoshida
Seiichi
S
Nishikawa
Masataka
M
Mori
Ikuko
I
Yanagisawa
Rie
R
Takano
Hirohisa
H
Inoue
Ken-ichiro
K
Sun
Guifan
G
Shibamoto
Takayuki
T
D000393:Air Pollutants / Q000633:toxicity*; D000818:Animals; D001992:Bronchoalveolar Lavage Fluid / Q000737:chemistry / Q000166:cytology; D002460:Cell Line; D018925:Chemokines / Q000378:metabolism; D002681:China; D004357:Drug Synergism; D004804:Eosinophils / Q000187:drug effects* / Q000473:pathology; D015870:Gene Expression / Q000187:drug effects; D006358:Hot Temperature; D007442:Intubation, Intratracheal; D008168:Lung / Q000187:drug effects* / Q000276:immunology / Q000473:pathology; D008264:Macrophages / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D008813:Mice, Inbred ICR; D010047:Ovalbumin / Q000008:administration & dosage / Q000276:immunology; D052638:Particulate Matter / Q000633:toxicity*; D011650:Pulmonary Alveoli / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D011657:Pulmonary Eosinophilia / Q000139:chemically induced* / Q000276:immunology / Q000473:pathology; D012333:RNA, Messenger / Q000378:metabolism; D051195:Toll-Like Receptor 2 / Q000235:genetics / Q000378:metabolism; D051197:Toll-Like Receptor 4 / Q000235:genetics / Q000378:metabolism
D000393:Air Pollutants; D018925:Chemokines; D052638:Particulate Matter; D012333:RNA, Messenger; C493486:Tlr2 protein, mouse; C493487:Tlr4 protein, mouse; D051195:Toll-Like Receptor 2; D051197:Toll-Like Receptor 4; D010047:Ovalbumin