CAJ | 학술논문

目的：观察和分析老年慢性阻塞性肺病（COPD）患者外周血单核细胞 TLR2，TLR4等 Toll 样受体（TLRs）的表达情况及其与炎症因子的关系。方法选取80例老年 COPD 患者，根据其病情将其分为 COPD 稳定期组和 AECOPD 组，分别为43例和37例患者。选取80例健康老年人，根据其是否吸烟分为吸烟组和不吸烟组，分别为41例和39例。对各组研究对象的外周血单核细胞表面 TLR2，TLR4表达水平和血清白细胞介素-6（IL-6），白细胞介素-8（IL-8）和肿瘤坏死因子-α（TNF-α）水平进行检测和比较。结果从 AECOPD 组、不吸烟组到 COPD 稳定期组，研究对象的外周血单核细胞表面 TLR2，TLR4表达水平依次显著升高，且 COPD 稳定期组患者的外周血单核细胞表面 TLR4表达水平显著高于吸烟组（q＝2.815～3.754，P ＜0.05）；从 AECOPD 组，COPD 稳定期组、吸烟组到不吸烟组，研究对象的血清 IL-6，TNF-α水平依次显著降低且 AECOPD 组患者的血清 IL-8水平显著高于其他三组（q＝5.247～8.175，P ＜0.05）；COPD 患者外周血单核细胞表面 TLR2的表达水平与血清 IL-6水平（标化回归系数＝0.458）、血清 IL-8水平（标化回归系数＝0.622）和血清TNF-α水平（标化回归系数＝0.562）具有相关性（P ＜0.05），TLR4的表达水平与血清 IL-6水平（标化回归系数＝0.478）、血清 IL-8水平（标化回归系数＝0.569）和血清 TNF-α水平（标化回归系数＝0.352）具有相关性（P ＜0.05）。结论老年COPD 患者的外周血单核细胞表面的 TLR2，TLR4等 TLRs 呈现过表达状态，这与患者血清炎症因子水平的上升具有密切的相关性，TLRs 的过表达参与了 COPD 发生和进展的过程。
목적：관찰화분석노년만성조새성폐병（COPD）환자외주혈단핵세포 TLR2，TLR4등 Toll 양수체（TLRs）적표체정황급기여염증인자적관계。방법선취80례노년 COPD 환자，근거기병정장기분위 COPD 은정기조화 AECOPD 조，분별위43례화37례환자。선취80례건강노년인，근거기시부흡연분위흡연조화불흡연조，분별위41례화39례。대각조연구대상적외주혈단핵세포표면 TLR2，TLR4표체수평화혈청백세포개소-6（IL-6），백세포개소-8（IL-8）화종류배사인자-α（TNF-α）수평진행검측화비교。결과종 AECOPD 조、불흡연조도 COPD 은정기조，연구대상적외주혈단핵세포표면 TLR2，TLR4표체수평의차현저승고，차 COPD 은정기조환자적외주혈단핵세포표면 TLR4표체수평현저고우흡연조（q＝2.815～3.754，P ＜0.05）；종 AECOPD 조，COPD 은정기조、흡연조도불흡연조，연구대상적혈청 IL-6，TNF-α수평의차현저강저차 AECOPD 조환자적혈청 IL-8수평현저고우기타삼조（q＝5.247～8.175，P ＜0.05）；COPD 환자외주혈단핵세포표면 TLR2적표체수평여혈청 IL-6수평（표화회귀계수＝0.458）、혈청 IL-8수평（표화회귀계수＝0.622）화혈청TNF-α수평（표화회귀계수＝0.562）구유상관성（P ＜0.05），TLR4적표체수평여혈청 IL-6수평（표화회귀계수＝0.478）、혈청 IL-8수평（표화회귀계수＝0.569）화혈청 TNF-α수평（표화회귀계수＝0.352）구유상관성（P ＜0.05）。결론노년COPD 환자적외주혈단핵세포표면적 TLR2，TLR4등 TLRs 정현과표체상태，저여환자혈청염증인자수평적상승구유밀절적상관성，TLRs 적과표체삼여료 COPD 발생화진전적과정。
Objective To observe and analyze the expressions of Toll like receptors (TLRs)of TLR2,TLR4 in peripheral blood mononuclear cells and its correlation with the inflammatory factors levels of the elderly patients with chronic obstruc-tive pulmonary disease (COPD).Methods 80 cases of elderly patients with COPD were selected and divided into the COPD stable phase group and the AECOPD group according to their condition of diseases.43 patients and 37 patients were included into each group respectively.80 cases of healthy elderly people were selected and divided into the smoking group and the non smoking group.41 cases and 39 cases were included into each group respectively.The expression levels of TLR2,TLR4 in peripheral blood mononuclear cells and the serum levels of interleukin-6 (IL-6),interleukin-8 (IL-8),tumor necrosis factor-α(TNF-α)of the objects in all the groups were detected and compared.Results From the AECOPD group,the non smoking group to the COPD stable phase group,the expression levels of TLR2,TLR4 in peripheral blood mononuclear cells of the objects increased significantly gradually and the TLR4 expression level in peripheral blood mononuclear cells of the patients in the COPD stable phase was significantly higher than that in the smoking group (q=2.815~3.754,P <0.05).From the AECOPD group,the COPD stable phase group,the smoking group to the non smoking group,the serum IL-6,TNF-αlevels of the objects decreased significantly gradually and the serum IL-8 level of the patients in the AECOPD group was signifi-cantly higher than that of the other three group (q=5.247~8.175,P <0.05).The expression level of TLR2 in peripheral blood mononuclear cells of COPD patients was correlated with the serum IL-6 level (standardized regression coefficient=0.458),the serum IL-8 level (standardized regression coefficient=0.622)and the serum TNF-αlevel (standardized regres-sion coefficient=0.562)(P <0.05),the expression of TLR4 was correlated with the serum IL-6 level (standard the regres-sion coefficient= 0.478),the serum IL-8 level (standardized regression coefficient= 0.569)and the serum TNF-α level (standardized regression coefficient=0.352)(P <0.05).Conclusion The elderly patients with COPD showed the overex-pression state of TLRs of TLR2,TLR4 in the peripheral blood mononuclear cells.Such increases were correlated closely with the serum levels of the inflammatory factors in the patients.The overexpression of TLRs should involve in the occur-rence and the progression of COPD.