Ym1 and Ym2 expression in a mouse model exposed to diesel exhaust particles

• DOI: 10.1002/tox.20319
• Publication Date: 2008-01-23T19:16:56Z
• Authors: Hyun‐Mi Song; An‐Soo Jang; Mi‐Hyun Ahn; Hajime Takizawa; Shin‐Hwa Lee; Ji‐Hee Kwon; Young‐Mok Lee; TaiYoun Rhim; Choon‐Sik Park
• Keywords: 0301 basic medicine; Air Pollutants; Inhalation Exposure; Mice, Inbred BALB C; Reverse Transcriptase Polymerase Chain Reaction; Chitinases; Gene Expression; Asthma; Specific Pathogen-Free Organisms; 3. Good health; Disease Models, Animal; Mice; 03 medical and health sciences; Lectins; Animals; Female; Interleukin-4; RNA, Messenger; Particle Size; Bronchoalveolar Lavage Fluid; Gasoline; Methacholine Chloride; Environmental Monitoring

AbstractBackground: Chitinase may play a role in regulating allergic diseases. Objective: We studied the role of chitinase in a mouse model exposed to diesel exhaust particles (DEP). Mice were exposed to intranasal DEP (0.6 mg/mL) for 5 days and challenged with aerosolized DEP (6 mg/m3) on days 6–8. Enhanced pause (Penh), as an airway obstruction marker, was measured on day 9, and bronchoalveolar lavage (BAL) fluid and lung tissues were collected on day 10. The expression of Ym1 and Ym2 mRNA was assessed in lung tissue extracts by reverse transcription‐polymerase chain reaction. Results: DEP induced significant increases in methacholine‐induced Penh and IL‐4 levels in BAL fluid relative to the control group. Peribronchial and perivascular inflammatory cell infiltrates were prominent in the DEP group. DEP induced Ym1 and Ym2 mRNA expression in lung tissue extracts relative to the control group. Conclusion: These results demonstrate that DEP induced airway hyperresponsiveness and Ym mRNA expression via a Th2 cell‐biased response, suggesting that chitinase may play an important role in airway inflammation and responsiveness upon exposure to DEP in a mouse model, and may therefore be involved in regulating allergic diseases. © 2008 Wiley Periodicals, Inc. Environ Toxicol, 2008.