【摘要】：目的了解樹突狀細(xì)胞表面因子OX62、CD83在慢阻肺大鼠肺部的表達(dá)變化,并探討CCL20抗體的干預(yù)作用。方法選用30只健康Wistar大鼠,隨機(jī)分為健康對(duì)照組(10只)、慢阻肺模型組(10只)、CCL20單抗組(10只),用氣道內(nèi)注入脂多糖(共2次)聯(lián)合煙霧刺激(約28 d)的方法誘導(dǎo)慢阻肺模型。在實(shí)驗(yàn)初始對(duì)單抗組大鼠以CCL20單克隆抗體腹腔注射一次。在第29天取大鼠的肺組織觀察其病理學(xué)改變,用免疫組織化學(xué)技術(shù)檢測肺部樹突狀細(xì)胞(DC)的表面因子OX62、CD83的表達(dá)變化。結(jié)果模型組大鼠肺組織HE染色符合氣道炎癥和肺氣腫的表現(xiàn),CCL20單抗組大鼠肺部病理表現(xiàn)比慢阻肺組明顯減輕。與健康對(duì)照組相比,慢阻肺模型組大鼠的肺組織中OX62的表達(dá)比對(duì)照組明顯增多(P0.05),而在CCL20單抗組低于慢阻肺組(P0.05)。慢阻肺模型組大鼠肺組織中CD83的表達(dá)比對(duì)照組少(P0.05),而在慢阻肺組與CCL20單抗組之間則沒有明顯的差異(P0.05)。結(jié)論慢阻肺的發(fā)病可能與肺部OX62的表達(dá)增多及CD83的表達(dá)減少有關(guān),使用CCL20單抗能部分地抑制這一效應(yīng)。
[Abstract]:Objective to investigate the expression of dendritic cell surface factor (OX62,CD83) in lung of COPD rats and to explore the effect of CCL20 antibody. Methods Thirty healthy Wistar rats were randomly divided into control group (n = 10), chronic obstructive pulmonary model group (n = 10) and CCL20 monoclonal antibody group (n = 10). The model of chronic obstructive lung was induced by intratracheal injection of lipopolysaccharide (2 times) combined with smoke stimulation (about 28 days). At the beginning of the experiment, the rats in the monoclonal antibody group were injected intraperitoneally with CCL20 monoclonal antibody. The pathological changes of lung tissue were observed on the 29th day, and the expression of surface factor OX62,CD83 of (DC) in dendritic cells was detected by immunohistochemistry. Results HE staining in lung tissue of model group was consistent with the manifestations of airway inflammation and emphysema. The pathological manifestations of lung in CCL20 monoclonal antibody group were significantly less than those in slow obstructive lung group. Compared with the healthy control group, the expression of OX62 in the lung tissue of the COPD model group was significantly higher than that of the control group (P0.05), while the expression of OX62 in the CCL20 monoclonal antibody group was lower than that in the COPD group (P0.05). The expression of CD83 in the lung tissue of the COPD model group was lower than that of the control group (P0.05), but there was no significant difference between the COPD group and the CCL20 monoclonal antibody group (P0.05). Conclusion the pathogenesis of COPD may be related to the increase of OX62 expression and the decrease of CD83 expression, which can be partly inhibited by the use of CCL20 monoclonal antibody.
【作者單位】： 遵義醫(yī)學(xué)院附屬醫(yī)院呼吸一科;華中科技大學(xué)同濟(jì)醫(yī)學(xué)院附屬同濟(jì)醫(yī)院呼吸與危重癥醫(yī)學(xué)科衛(wèi)生部呼吸系統(tǒng)疾病重點(diǎn)實(shí)驗(yàn)室;
【基金】：國家自然科學(xué)基金(81460008)
【分類號(hào)】：R563.9

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