Mo Bi-Wen, Zhang Zhen-Zhen, Wei Jiang-Hong, Huang Jian-Wei, Mo Bi-Fan, Wang Chang-Ming, Zeng Jin-Rong, Xu Qing, Lin Yun
Department of Respiratory Medicine, Hospital Affiliated Guilin Medical College, Guilin 541001, China.
Zhongguo Ying Yong Sheng Li Xue Za Zhi. 2013 Mar;29(2):153-7.
To investigate the effects of lipopolysaccharide (LPS) on airway inflammation, airway remodeling and the expression of Toll-like receptor 4 (TLR4) mRNA in asthmatic rats.
Twenty-four SPF level SD rats were randomly divided into four groups (n = 6): control group, low dose of LPS group, high dose of LPS group and asthma group. Using ovalbumin (OVA) to sensitize and challenge to establish asthmatic rat model. Observed pathological changes of lung tissue by HE staining, inflammatory cell infiltration was observed by airway wall eosinophils (EOS) counts; airway resistance was determined; image analysis software was used to determine the thickness of airway wall, detected airway smooth muscle TLR4 expression levels by RT-PCR.
The rat airway resistance and the EOS number of airway wall and the thickness of airway wall in asthma group, low dose of LPS group and high dose of LPS group were significantly higher than those in control group (P < 0.01). The above-mentioned parameters of high dose of LPS group showed significantly lower than those in asthma group and low dose of LPS group (P < 0.05). The expression of rat airway smooth muscle TLR4 mRNA in low dose of LPS group and high dose of LPS group were significantly higher than those in asthma group (P < 0.01). And the expression of rat airway smooth muscle TLR4 mRNA in high dose of LPS group was significantly higher than that in low dose of LPS group (P < 0.05).
TLR4 plays an important role in asthmatic airway inflammation and airway remodeling, LPS may play double-sided regulation in asthmatic airway inflammation and airway remodeling by activated TLR4.
探讨脂多糖(LPS)对哮喘大鼠气道炎症、气道重塑及Toll样受体4(TLR4)mRNA表达的影响。
将24只SPF级SD大鼠随机分为四组(n = 6):对照组、低剂量LPS组、高剂量LPS组和哮喘组。采用卵清蛋白(OVA)致敏和激发建立哮喘大鼠模型。通过HE染色观察肺组织病理变化,通过气道壁嗜酸性粒细胞(EOS)计数观察炎症细胞浸润;测定气道阻力;使用图像分析软件测定气道壁厚度,通过RT-PCR检测气道平滑肌TLR4表达水平。
哮喘组、低剂量LPS组和高剂量LPS组大鼠气道阻力、气道壁EOS数量及气道壁厚度均显著高于对照组(P < 0.01)。高剂量LPS组上述指标均显著低于哮喘组和低剂量LPS组(P < 0.05)。低剂量LPS组和高剂量LPS组大鼠气道平滑肌TLR4 mRNA表达均显著高于哮喘组(P < 0.01)。且高剂量LPS组大鼠气道平滑肌TLR4 mRNA表达显著高于低剂量LPS组(P < 0.05)。
TLR4在哮喘气道炎症和气道重塑中起重要作用,LPS可能通过激活TLR4对哮喘气道炎症和气道重塑发挥双向调节作用。