Airborne Asian sand dust enhances murine lung eosinophilia.
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.
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 / 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
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