目的探讨早产新生儿呼吸窘迫综合征(NRDS)中血清E-选择素(CD62E)、白介素-17(IL-17)表达水平及其与发病风险、病情程度的关系。方法选取2017年1月~2019年12月本院诊治的NRDS早产儿78例为NRDS组,无NRDS的60例早产儿为对照组。观察NRDS组...目的探讨早产新生儿呼吸窘迫综合征(NRDS)中血清E-选择素(CD62E)、白介素-17(IL-17)表达水平及其与发病风险、病情程度的关系。方法选取2017年1月~2019年12月本院诊治的NRDS早产儿78例为NRDS组,无NRDS的60例早产儿为对照组。观察NRDS组血清CD62E、IL-17水平与对照组的对比结果,分析CD62E、IL-17对早产儿NRDS的影响;比较不同病情的NRDS早产儿CD62E、IL-17水平,分析CD62E、IL-17与病情相关性。结果NRDS组血清CD62E为(37.29±18.95)ng/mL,IL-17为(101.63±52.31)ng/L,均高于对照组[CD62E为(17.77±8.42)ng/mL、IL-17为(61.10±24.98)ng/L],差异有统计学意义(P<0.05)。Logistic结果显示:CD62E(OR=1.111,95%CI=1.063~1.162)、IL-17(OR=1.012,95%CI=1.001~1.023)是早产儿发生NRDS的独立危险因素(P<0.05)。进一步ROC曲线显示:CD62E、IL-17诊断早产儿NRDS的AUC为0.836(95%CI=0.770~0.902)、0.732(95%CI=0.645~0.819)(均>0.7);CD62E敏感度、特异度依次为75.6%、81.7%,IL-17依次为56.4%、98.3%;CD62E、IL-17最佳临界值为24.5ng/mL、102.5ng/L;而两项联合诊断的AUC(95%CI)为0.875(95%CI=0.815~0.934),敏感度、特异度依次为78.2%、91.7%。重度NRDS早产儿血清CD62E(55.47±21.89 vs 39.26±12.61,ng/mL)、IL-17(147.47±27.00 vs 116.31±39.75,ng/L)高于中度患儿,中度患儿血清CD62E(39.26±12.61 vs 19.77±8.25,ng/mL)、IL-17(116.31±39.75 vs 40.18±23.68,ng/L)高于轻度患儿,差异有统计学意义(P<0.05)。Pearson相关性显示:CD62E、IL-17与早产儿NRDS病情程度均正相关(r=0.671、0.747,P<0.05)。结论血清CD62E、IL-17在NRDS早产儿中呈相对高表达,CD62E、IL-17水平增高的早产儿发生NRDS的风险更大,且CD62E、IL-17具有诊断NRDS与病情评估价值。展开更多
Idiopathic pulmonary fibrosis(IPF)is a fatal chronic interstitial lung disease with no established treatment and is characterized by progressive scarring of the lung tissue and an irreversible decline in lung function...Idiopathic pulmonary fibrosis(IPF)is a fatal chronic interstitial lung disease with no established treatment and is characterized by progressive scarring of the lung tissue and an irreversible decline in lung function.Chronic inflammation has been demonstrated to be the pathological basis of fibrosis.Emerging studies have revealed that most interleukin-17(IL-17)isoforms are essential for the mediation of acute and chronic inflammation via innate and adaptive immunity.Overexpression or aberrant expression of IL-17 cytokines contributes to various pathological outcomes,including the initiation and exacerbation of IPF.Here,we aim to provide an overview of IL-17 family members in the pathogenesis of IPF.展开更多
文摘目的探讨早产新生儿呼吸窘迫综合征(NRDS)中血清E-选择素(CD62E)、白介素-17(IL-17)表达水平及其与发病风险、病情程度的关系。方法选取2017年1月~2019年12月本院诊治的NRDS早产儿78例为NRDS组,无NRDS的60例早产儿为对照组。观察NRDS组血清CD62E、IL-17水平与对照组的对比结果,分析CD62E、IL-17对早产儿NRDS的影响;比较不同病情的NRDS早产儿CD62E、IL-17水平,分析CD62E、IL-17与病情相关性。结果NRDS组血清CD62E为(37.29±18.95)ng/mL,IL-17为(101.63±52.31)ng/L,均高于对照组[CD62E为(17.77±8.42)ng/mL、IL-17为(61.10±24.98)ng/L],差异有统计学意义(P<0.05)。Logistic结果显示:CD62E(OR=1.111,95%CI=1.063~1.162)、IL-17(OR=1.012,95%CI=1.001~1.023)是早产儿发生NRDS的独立危险因素(P<0.05)。进一步ROC曲线显示:CD62E、IL-17诊断早产儿NRDS的AUC为0.836(95%CI=0.770~0.902)、0.732(95%CI=0.645~0.819)(均>0.7);CD62E敏感度、特异度依次为75.6%、81.7%,IL-17依次为56.4%、98.3%;CD62E、IL-17最佳临界值为24.5ng/mL、102.5ng/L;而两项联合诊断的AUC(95%CI)为0.875(95%CI=0.815~0.934),敏感度、特异度依次为78.2%、91.7%。重度NRDS早产儿血清CD62E(55.47±21.89 vs 39.26±12.61,ng/mL)、IL-17(147.47±27.00 vs 116.31±39.75,ng/L)高于中度患儿,中度患儿血清CD62E(39.26±12.61 vs 19.77±8.25,ng/mL)、IL-17(116.31±39.75 vs 40.18±23.68,ng/L)高于轻度患儿,差异有统计学意义(P<0.05)。Pearson相关性显示:CD62E、IL-17与早产儿NRDS病情程度均正相关(r=0.671、0.747,P<0.05)。结论血清CD62E、IL-17在NRDS早产儿中呈相对高表达,CD62E、IL-17水平增高的早产儿发生NRDS的风险更大,且CD62E、IL-17具有诊断NRDS与病情评估价值。
基金Natural Science Foundation of Jiangsu Province(BK20180616)the Joint Funds for the Health and Education of Fujian Province(2019-WJ-31)the Institute of Respiratory Diseases,Xiamen Medical College(HXJB-15).
文摘Idiopathic pulmonary fibrosis(IPF)is a fatal chronic interstitial lung disease with no established treatment and is characterized by progressive scarring of the lung tissue and an irreversible decline in lung function.Chronic inflammation has been demonstrated to be the pathological basis of fibrosis.Emerging studies have revealed that most interleukin-17(IL-17)isoforms are essential for the mediation of acute and chronic inflammation via innate and adaptive immunity.Overexpression or aberrant expression of IL-17 cytokines contributes to various pathological outcomes,including the initiation and exacerbation of IPF.Here,we aim to provide an overview of IL-17 family members in the pathogenesis of IPF.