COPD患者TLR-4表達(dá)與氣道炎癥及氣道粘液高分泌的研究
發(fā)布時間:2018-03-31 05:14
本文選題:肺疾病 切入點(diǎn):慢性阻塞性 出處:《青島大學(xué)》2012年碩士論文
【摘要】:目的:檢測慢性阻塞性肺病患者肺組織中TLR-4, HBD-2, IL-8, MUC5AC的表達(dá),并探討TLR-4在氣道炎癥、氣道粘液高分泌中的作用。 方法:收集40例男性肺癌患者手術(shù)切除標(biāo)本,根據(jù)肺功能結(jié)果分為COPD組(20人)及非COPD組(20人),取其肺葉切除后的遠(yuǎn)離癌變部位的肺組織,對肺組織標(biāo)本行HE、AB-PAS染色,顯微鏡下觀察肺組織基本形態(tài)結(jié)構(gòu),對氣道炎癥細(xì)胞進(jìn)行評分,用免疫組織化學(xué)方法檢測肺組織中TLR-4, IL-8, HBD-2, MUC5AC的表達(dá)并分析其相關(guān)性。 結(jié)果:①COPD組出現(xiàn)明顯氣道炎癥細(xì)胞浸潤,COPD組氣道炎癥細(xì)胞評分(2.67±0.26)較對照組(1.15±0.34)增加(P0.05)。肺功能正常吸煙者與非吸煙者氣道炎癥細(xì)胞評分分別為(1.49±0.36,0.82±0.04),肺功能正常吸煙者氣道炎癥細(xì)胞評分較非吸煙者增加(P0.05), COPD組氣道上皮杯狀細(xì)胞百分比(27.83±6.72)較對照組(12.67±4.12)增加(P0.05)。COPD患者氣道MUC5AC主要表達(dá)于氣道杯狀細(xì)胞,COPD組及對照組氣道MUC5AC陽性率分別為(24.16±3.63) COPD組較對照組增高(16.12±4.41, P0.05).②COPD組肺組織中TLR-4、 HBD-2及IL一8表達(dá)的IOD值(分別為1110.12±302.61,1480.23±292.51,1496.41±346.86)較對照組(分別為724.21±242.13,864.31±121.53,654.46±215.16)增高(P0.05)。TLR-4主要表達(dá)在氣道壁及其周圍浸潤的單核一巨噬細(xì)胞、中性粒細(xì)胞,氣道上皮細(xì)胞、支氣管平滑肌細(xì)胞、血管內(nèi)皮細(xì)胞也有表達(dá),HBD-2主要表達(dá)于氣道上皮細(xì)胞,IL-8在氣道壁及其周圍浸潤的淋巴細(xì)胞、巨噬細(xì)胞、中性粒細(xì)胞均有表達(dá)。③吸煙組氣道炎癥細(xì)胞評分、杯狀細(xì)胞百分比、MUC5AC陽性率(分別為2.67+0.28,64.12±1.13,32.43+1.21)較非吸煙組(1.02±0.14,30.12±1.13,12.98±1.76)增高(P0.05)。④相關(guān)性分析:TLR-4表達(dá)與氣道中性粒細(xì)胞百分比、IL-8及HBD-2表達(dá)成正相關(guān)(r值分別是0.81、0.92、0.80,P均0.05),TLR-4表達(dá)與氣道MUC5AC表達(dá)成正相關(guān)(r為0.74,P0.05),IL-8與MUC5AC表達(dá)成正相關(guān)(r為0.82, P0.05), IL-8與氣道中性粒細(xì)胞及淋巴細(xì)胞百分比成正相關(guān)(r為0.94、0.78,P0.05)。氣道炎癥評分、杯狀細(xì)胞百分比及MUC5AC陽性率與吸煙指數(shù)呈正相關(guān)(r值分別為0.86、0.89、0.81,P0.05)。 結(jié)論:COPD患者氣道中TLR-4表達(dá)上調(diào)誘導(dǎo)HBD-2、IL-8表達(dá)增加,參與了COPD氣道炎癥反應(yīng),HBD-2作為TLR-4的內(nèi)源性配體可導(dǎo)致COPD氣道炎癥反應(yīng)放大,COPD患者M(jìn)UC5AC主要由杯狀細(xì)胞細(xì)胞產(chǎn)生,TLR-4通過間接誘導(dǎo)MUC5A表達(dá)參與氣道粘液高分泌。
[Abstract]:Aim: to detect the expression of TLR-4, HBD-2, IL-8, MUC5AC in pulmonary tissue of patients with chronic obstructive pulmonary disease (COPD), and to investigate the role of TLR-4 in airway inflammation and airway mucus hypersecretion.Methods: 40 male patients with lung cancer were divided into COPD group (n = 20) and non-#en1# group (n = 20) according to the results of lung function.The expression of TLR-4, IL-8, HBD-2 and MUC5AC in lung tissue was detected by immunohistochemical method and the correlation was analyzed.Results the score of airway inflammatory cells in the COPD group (2.67 鹵0.26) was higher than that in the control group (1.15 鹵0.34).The scores of airway inflammatory cells in normal lung function smokers and non-smokers were 1.49 鹵0.36 鹵0.82 鹵0.04g, respectively. The airway inflammatory cell score of normal smokers was higher than that of non-smokers (P 0.05). The percentage of goblet cells in airway epithelium in COPD group was 27.83 鹵6.72), which was higher than that in control group (12.67 鹵4.12).(724.21 鹵242.13864.31 鹵121.53654.46 鹵215.16) the expression of P0.05U. TLR-4 was mainly expressed in mononuclear macrophages infiltrated in the airway wall and surrounding airway wall.The expression of HBD-2 in neutrophilic granulocytes, airway epithelial cells, bronchial smooth muscle cells and vascular endothelial cells was mainly expressed in lymphocytes and macrophages infiltrated in and around the airway wall of airway epithelial cells.Neutrophil expression 3. 3 in smoking group, airway inflammatory cell score,The positive correlation between IL-8 expression and MUC5AC expression was 0.82, P 0.05, and the positive correlation between IL-8 and the percentage of airway neutrophils and lymphocytes was 0.94 ~ 0.78%.Airway inflammation score, goblet cell percentage and MUC5AC positive rate were positively correlated with smoking index.Conclusion the up-regulated expression of TLR-4 induces the increase of HBD-2 IL-8 expression in the airway of patients with TLR-4.As an endogenous ligand of TLR-4, HBD-2 involved in the airway inflammation response of COPD may induce MUC5AC to produce TLR-4 mainly by goblet cells and participate in airway mucus hypersecretion through indirect induction of MUC5A expression in COPD patients.
【學(xué)位授予單位】:青島大學(xué)
【學(xué)位級別】:碩士
【學(xué)位授予年份】:2012
【分類號】:R563.9
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