目的:分析IL-6和趋化因子CCL2与前列腺癌及其骨转移的关系,评估诊断价值。方法:检测比较前列腺癌患者(包括发生骨转移及未发生骨转移者)、前列腺增生患者、正常对照者血清IL-6、CCL2水平,通过受试者工作特征(Receiver Operating Charact...目的:分析IL-6和趋化因子CCL2与前列腺癌及其骨转移的关系,评估诊断价值。方法:检测比较前列腺癌患者(包括发生骨转移及未发生骨转移者)、前列腺增生患者、正常对照者血清IL-6、CCL2水平,通过受试者工作特征(Receiver Operating Characteristic,ROC)曲线评估IL-6和CCL2单独及联合诊断前列腺癌及其骨转移的价值。结果:对血清IL-6、CCL2水平而言,前列腺癌患者显著高于前列腺增生患者,前列腺增生患者显著高于正常对照组者,发生骨转移者显著高于未发生骨转移者;IL-6、CCL2联合诊断前列腺癌及其骨转移的AUC显著高于单独诊断(前列腺癌:0.911 vs 0.718、0.691,P均<0.001,骨转移:0.909 vs 0.714、0.693,P=0.048、0.046),灵敏度、特异度分别为81.8%、90.3%与88.9%、87.0%。结论:IL-6和CCL2联合检测可以应用于前列腺癌及其骨转移的诊断。展开更多
Spinal cord injury causes accumulation of a large number of leukocytes at the lesion site where they contribute to excessive inflammation.Overproduced chemokines are responsible for the migratory process of the leukoc...Spinal cord injury causes accumulation of a large number of leukocytes at the lesion site where they contribute to excessive inflammation.Overproduced chemokines are responsible for the migratory process of the leukocytes,but the regulatory mechanism underlying the production of chemokines from resident cells of the spinal cord has not been fully elucidated.We examined the protein levels of macrophage migration inhibitory factor and chemokine C-C motif chemokine ligand 2 in a spinal cord contusion model at different time points following spinal cord injury.The elevation of macrophage migration inhibitory factor at the lesion site coincided with the increase of chemokine C-C motif chemokine ligand 2 abundance in astrocytes.Stimulation of primary cultured astrocytes with different concentrations of macrophage migration inhibitory factor recombinant protein induced chemokine C-C motif chemokine ligand 2 production from the cells,and the macrophage migration inhibitory factor inhibitor 4-iodo-6-phenylpyrimidine attenuated the stimulatory effect.Further investigation into the underlying mechanism on macrophage migration inhibitory factor-mediated astrocytic production of chemokine C-C motif chemokine ligand 2 revealed that macrophage migration inhibitory factor activated intracellular JNK signaling through binding with CD74 receptor.Administration of the macrophage migration inhibitory factor inhibitor 4-iodo-6-phenylpyrimidine following spinal cord injury resulted in the reduction of chemokine C-C motif chemokine ligand 2-recruited microglia/macrophages at the lesion site and remarkably improved the hindlimb locomotor function of rats.Our results have provided insights into the functions of astrocyte-activated chemokines in the recruitment of leukocytes and may be beneficial to develop interventions targeting chemokine C-C motif chemokine ligand 2 for neuroinflammation after spinal cord injury.展开更多
文摘目的:分析IL-6和趋化因子CCL2与前列腺癌及其骨转移的关系,评估诊断价值。方法:检测比较前列腺癌患者(包括发生骨转移及未发生骨转移者)、前列腺增生患者、正常对照者血清IL-6、CCL2水平,通过受试者工作特征(Receiver Operating Characteristic,ROC)曲线评估IL-6和CCL2单独及联合诊断前列腺癌及其骨转移的价值。结果:对血清IL-6、CCL2水平而言,前列腺癌患者显著高于前列腺增生患者,前列腺增生患者显著高于正常对照组者,发生骨转移者显著高于未发生骨转移者;IL-6、CCL2联合诊断前列腺癌及其骨转移的AUC显著高于单独诊断(前列腺癌:0.911 vs 0.718、0.691,P均<0.001,骨转移:0.909 vs 0.714、0.693,P=0.048、0.046),灵敏度、特异度分别为81.8%、90.3%与88.9%、87.0%。结论:IL-6和CCL2联合检测可以应用于前列腺癌及其骨转移的诊断。
基金supported by the China Postdoctoral Science Foundation,No.2020M681689(to YMH)the Basic Scientific Research Projects of Nantong,Nos.JC2020015(to HX)and JC2020041(to YMH)。
文摘Spinal cord injury causes accumulation of a large number of leukocytes at the lesion site where they contribute to excessive inflammation.Overproduced chemokines are responsible for the migratory process of the leukocytes,but the regulatory mechanism underlying the production of chemokines from resident cells of the spinal cord has not been fully elucidated.We examined the protein levels of macrophage migration inhibitory factor and chemokine C-C motif chemokine ligand 2 in a spinal cord contusion model at different time points following spinal cord injury.The elevation of macrophage migration inhibitory factor at the lesion site coincided with the increase of chemokine C-C motif chemokine ligand 2 abundance in astrocytes.Stimulation of primary cultured astrocytes with different concentrations of macrophage migration inhibitory factor recombinant protein induced chemokine C-C motif chemokine ligand 2 production from the cells,and the macrophage migration inhibitory factor inhibitor 4-iodo-6-phenylpyrimidine attenuated the stimulatory effect.Further investigation into the underlying mechanism on macrophage migration inhibitory factor-mediated astrocytic production of chemokine C-C motif chemokine ligand 2 revealed that macrophage migration inhibitory factor activated intracellular JNK signaling through binding with CD74 receptor.Administration of the macrophage migration inhibitory factor inhibitor 4-iodo-6-phenylpyrimidine following spinal cord injury resulted in the reduction of chemokine C-C motif chemokine ligand 2-recruited microglia/macrophages at the lesion site and remarkably improved the hindlimb locomotor function of rats.Our results have provided insights into the functions of astrocyte-activated chemokines in the recruitment of leukocytes and may be beneficial to develop interventions targeting chemokine C-C motif chemokine ligand 2 for neuroinflammation after spinal cord injury.
