LPS对支气管哮喘气道炎症中ASC表达的影响

Effects of LPS on ASC expression in the lung tissue of mice with bronchial asthma's airway inflammation

目的探讨凋亡相关点样蛋白（apoptoticspeck-likeproteincontainingacaspaserecruitmentdomain，ASC）在支气管哮喘小鼠肺组织中的表达情况，以及脂多糖（1ipopolysaccharide，LPS）对其的调节作用。方法SPF级雌性C57BLt6小鼠24只，6～8周．18-20g／只，随机分为3组，分别为PBS对照组（A）、哮喘组（B）、LPS干预组（C）。B、C组小鼠以卵蛋白（OVA）致敏并激发，其中C组在激发前给予10μg/只的LPS腹腔注射，连续3d；A组用PBS溶液替代OVA致敏和激发。末次激发24h后，记录各组小鼠的气道反应性监测指标增强呼气间歇（Penh）值。取右上肺组织常规HE染色，光学显微镜下观察组织形态，气管和血管周围炎症细胞浸润情况；行ASC免疫组化，观察其在各组肺组织中的分布情况。采用方差分析进行多组间比较。结果对比A、B组小鼠行为学变化、气道反应性及肺组织病理，显示哮喘小鼠造模成功；C组气道反应性[（1．75±0．46）至（6．53±0．81）1较B组[（4．05±0．22）至（12．07±0．91）]下降，差异有统计学意义（P〈O．05）；免疫组化提示ASC在哮喘模型中较对照组高表达，而10μg的LPS可明显增加哮喘小鼠中气道上皮的ASC表达。结论ASC参与哮喘中炎症反应的发生：一定剂量的LPS可加重哮喘小鼠气道上皮炎症，增强ASC在炎症中的参与，但降低哮喘小鼠气道高反应性。

To investigate the expression of the apoptotic speck-like protein containing a caspase recruitment domain （ASC） in the lung tissue of mice with bronchial asthma, 24 SPF female mice were randomly divided into PBS control group （A）, OVA-induced asthma group （B）, and LPS pre-treatment ＋ OVA-induced asthma group （C）. Groups B and C received OVA injection of sensitization and challenge. The mice in group C were intraperitoneally injected with 10 μg of lipopolysaccharide （LPS） 3 days before challenge. Group A were sensitized with PBS instead of OVA. Airway reactivity of each mouse was measured using BUXCO noninvasive detector 24 hours after last challenge. At last the morphological changes, inflammatory cell infiltration over and alongside the trachea and blood vessel of right lung biopsy specimens were observed by HE stainning. Compared with group A, group B demonstrated behavioral changes, airway reactivity, pathological changes of lung tissues, suggesting successful asthma induction in group B; the reaction of the esophagus decreased in group C [（1.75±0.46） to （6.53±0.81）] compared with group B [（4.05±0.22） to （12.07±0.91）] （P〈 0.05）. The expression of ASC in group A was higher than group B according to immunohistochemical result, but 10 μg of LPS injection stimulated the ASC expression of asthma airway epithelium of mice in group B. The ASC was likely to be involved in inflammation of mice with asthma. LPS injection aggravated inflammatory reactions in the airway epithelium, increased the number of inflammasome involved in inflammation reaction, but decreased airway hyperresponsiveness in mice with asthma.