Inoue Ken-Ichiro, Koike Eiko, Yanagisawa Rie, Takano Hirohisa
National Institute for Environmental Studies, Tsukuba, Ibaraki, Japan.
Immunopharmacol Immunotoxicol. 2009;31(1):71-4. doi: 10.1080/08923970802355835.
Although diesel exhaust particles (DEP) exacerbate murine allergic asthma, the mechanisms remain unclarified. This study elucidated the effects of pulmonary exposure to DEP on extrathoracic allergen-induced CD4 polarization using an ex vivo system in asthmatic mice. Mice were divided into 4 groups, and vehicle, DEP, ovalbumin (OVA), or DEP + OVA was intratracheally instilled biweekly 5 times. Twenty-four h after the last intratracheal instillation, the spleen was removed. Mononuclear cells were isolated from the spleen and stimulated in vitro with OVA; thereafter, the number of separated CD4(+) cells was counted. The number of separated CD4(+) cells was significantly greater in the OVA or the DEP + OVA group than in the vehicle group. Furthermore, the number was significantly greater in the DEP + OVA than in the DEP or the OVA group. Taken together, in vivo DEP exposure amplified extrathoracic CD4 polarization in asthmatic subjects.
尽管柴油废气颗粒(DEP)会加重小鼠过敏性哮喘,但相关机制仍不清楚。本研究利用哮喘小鼠的体外系统,阐明了肺部暴露于DEP对胸外过敏原诱导的CD4极化的影响。将小鼠分为4组,每两周经气管内滴注1次媒介物、DEP、卵清蛋白(OVA)或DEP + OVA,共5次。最后一次气管内滴注24小时后,取出脾脏。从脾脏中分离出单核细胞,并用OVA进行体外刺激;此后,对分离出的CD4(+)细胞数量进行计数。OVA组或DEP + OVA组中分离出的CD4(+)细胞数量显著多于媒介物组。此外,DEP + OVA组中的数量显著多于DEP组或OVA组。综上所述,体内DEP暴露会增强哮喘患者胸外CD4极化。