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백서에서 디젤분진이 기도염증과 과민성에 미치는 영향

Effects of Diesel Exhaust Particles on Airway Inflammation and Hyperresponsiveness in a Murine Model

박성우|김영은|이준혁|박춘식|장안수|안미현|임태연|송현미|신정아
대한천식알레르기학회 (The Korean Academy of Asthma, Allergy and Clinical Immunology)|2005.06|천식 및 알레르기|제25권 제2호|pp. 117-122

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참고문헌

주제분류임상병리학

초록

Abstract

Background: Epidemiologic studies show that increases in diesel exhaust particles (DEP) can aggravate acute asthma. However, there were a few asthma models in mice exposed to DEP. Nitric oxide (NO) may contributeto airway inflammation and hyperresponsiveness (AHR). Objective: We have determined the effects of DEP on AHR and inflammation using a mouse model. We have also investigated the effects of DEP on the production of NO in vivo and in vitro. Method: The mice were intra-nasally sensitized with 0.6 mg/mL of DEP for 5 days and were challenged with 6 mg/m3 of DEP by inhalation route for 3 days. The mice were subjected to whole-body plethysmography and killed for performance of bronchoalveolar lavage and histology. Murine macrophage cell line, Raw 264.7 cellswere exposed to 50μg/mL of DEP and nitrate levels in the culture super-natants were measured with the Griess reagent. Expression of NO synthase was detected by RT-PCR. Result: DEP induced a significant increase in methacholine- induced AHR. The levels of IL-4 and eotaxin increased in the BAL fluid in mice exposed to DEP. DEP stimulated nitrite production in the BAL fluid. Nitrite increased in Raw 264.7 cells exposed to DEP. DEP stimulated the expression of iNOS in lung tissue in mice exposed to DEP. Alveolar macrophage was expressed iNOS mRNA 24 h and 48 h after stimulation with DEP in vitro with peak time in 48 h post- stimulation. Conclusion: It is suggested that DEP may induce AHR and produce NO, and that NO may be an important role in airway inflammation by DEP.

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