CAJ | 학술논문

目的观察脓毒症患者外周血单核细胞CD14+CD16-、CD14+CD16+、CD14-CD16+三个亚群表达HLA-DR、CD14、CD16的异同，并分析CD14+CD16+单核细胞的特点。方法选取67例脓毒症患者为脓毒症组和15例健康志愿者作为对照组，脓毒症组根据疾病严重程度分为脓毒症（15例）、重症脓毒症（41例）和脓毒性休克组（11例），收集临床资料，计算APACHE II评分，流式细胞仪检测单核细胞各亚群CD14、CD16、HLA-DR的表达。结果脓毒症患者CD14+CD16+单核细胞数目较正常对照组显著升高（P＜0.01）；脓毒症患者单核细胞HLA-DR、CD14平均荧光强度均较健康对照组明显降低，并随着脓毒症患者病情由轻到重而逐渐下降；各组中CD14+CD16+单核细胞相对高表达HLA-DR、CD14；单核细胞HLA-DR表达与临床指标间存在较好的相关关系。结论①脓毒症患者单核细胞HLA-DR表达显著降低；②CD14+CD16+单核细胞在脓毒症发病的免疫机制中可能起到重要作用。
목적관찰농독증환자외주혈단핵세포CD14+CD16-、CD14+CD16+、CD14-CD16+삼개아군표체HLA-DR、CD14、CD16적이동，병분석CD14+CD16+단핵세포적특점。방법선취67례농독증환자위농독증조화15례건강지원자작위대조조，농독증조근거질병엄중정도분위농독증（15례）、중증농독증（41례）화농독성휴극조（11례），수집림상자료，계산APACHE II평분，류식세포의검측단핵세포각아군CD14、CD16、HLA-DR적표체。결과농독증환자CD14+CD16+단핵세포수목교정상대조조현저승고（P＜0.01）；농독증환자단핵세포HLA-DR、CD14평균형광강도균교건강대조조명현강저，병수착농독증환자병정유경도중이축점하강；각조중CD14+CD16+단핵세포상대고표체HLA-DR、CD14；단핵세포HLA-DR표체여림상지표간존재교호적상관관계。결론①농독증환자단핵세포HLA-DR표체현저강저；②CD14+CD16+단핵세포재농독증발병적면역궤제중가능기도중요작용。
Objective To observe the expression of HLA-DR, CD14 and CD16 for the different subgroup of monocyte, and analyze the feather of CD14 +CD16 + monocyte. Methods Sixty-seven cases admitted to Emergency ICU and Surgery ICU of the hospital between March and August, 2009 were divided into sepsis group (n=15), severe sepsis group (n=41), and septic shock group (n=11), versus the control group of healthy people (n=15). The frequencies of CD14, CD16 and HLA-DR of monocyte were detected by flow cytometric analysis. Simultaneously, clinical data were collected and to calculate APACHE II scores. Results A significant increase in the number of CD14+CD16+monocyte of sepsis patients were observed compared with the control group;MFI of HLA-DR, CD14 were significantly lower of sepsis group than the control group, and MFI reflected lower with Exacerbations. HLA-DR and CD14 were highly expressed in CD14+CD16+ monocyte. HLA-DR expression of monocyte is mutually related with the clinical indicators. Conclusion ①HLA-DR Expression of monocyte in sepsis patients reflects significantly lower; ②CD14 +CD16 +monocyte might play a key role in the Immune pathogenesis of sepsis.