Song Hyun-Mi, Jang An-Soo, Ahn Mi-Hyun, Takizawa Hajime, Lee Shin-Hwa, Kwon Ji-Hee, Lee Young-Mok, Rhim Tai Youn, Park Choon-Sik
Department of Internal Medicine, Soonchunhyang University Hospital, Bucheon, Korea.
Environ Toxicol. 2008 Feb;23(1):110-6. doi: 10.1002/tox.20319.
Chitinase may play a role in regulating allergic diseases.
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/m(3)) 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.
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.
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.
几丁质酶可能在调节过敏性疾病中发挥作用。
我们在暴露于柴油废气颗粒(DEP)的小鼠模型中研究了几丁质酶的作用。小鼠经鼻内给予DEP(0.6mg/mL),持续5天,并在第6 - 8天用雾化DEP(6mg/m³)进行激发。在第9天测量作为气道阻塞标志物的增强暂停(Penh),并在第10天收集支气管肺泡灌洗(BAL)液和肺组织。通过逆转录 - 聚合酶链反应评估肺组织提取物中Ym1和Ym2 mRNA的表达。
与对照组相比,DEP导致乙酰甲胆碱诱导的Penh和BAL液中IL - 4水平显著升高。DEP组支气管周围和血管周围炎症细胞浸润明显。与对照组相比,DEP诱导肺组织提取物中Ym1和Ym2 mRNA表达。
这些结果表明,DEP通过偏向Th2细胞的反应诱导气道高反应性和Ym mRNA表达,提示几丁质酶在小鼠模型中暴露于DEP时可能在气道炎症和反应性中起重要作用,因此可能参与调节过敏性疾病。