目的:探讨嗜酸粒细胞活化趋化因子(eotaxin)与其相应受体CCR3的表达在慢性自发性荨麻疹发病中的作用。方法:采用酶联免疫吸附试验检测45例慢性自发性荨麻疹患者及30例正常人血清中eotaxin水平;同时用流式细胞仪分析外周血中CCR3的表达...目的:探讨嗜酸粒细胞活化趋化因子(eotaxin)与其相应受体CCR3的表达在慢性自发性荨麻疹发病中的作用。方法:采用酶联免疫吸附试验检测45例慢性自发性荨麻疹患者及30例正常人血清中eotaxin水平;同时用流式细胞仪分析外周血中CCR3的表达。结果:与正常对照组相比,患者组血清中eotaxin明显升高[(198.63±46.35)pg/m L vs(104.55±38.45)pg/m L];外周血CCR3表达水平显著增加[(38.24±6.87)%vs(20.37±5.40)%],差异均有统计学意义(t值分别为4.25、11.98,P值均<0.05)。结论:具有生物活性趋化因子及其受体介导的嗜酸性粒细胞的聚集、激活后释放的炎性介质在慢性自发性荨麻疹发病中起着重要作用。展开更多
Neuroinflammation and the NACHT,LRR,and PYD domains-containing protein 3 inflammasome play crucial roles in secondary tissue damage following an initial insult in patients with traumatic brain injury(TBI).Maraviroc,a ...Neuroinflammation and the NACHT,LRR,and PYD domains-containing protein 3 inflammasome play crucial roles in secondary tissue damage following an initial insult in patients with traumatic brain injury(TBI).Maraviroc,a C-C chemokine receptor type 5 antagonist,has been viewed as a new therapeutic strategy for many neuroinflammatory diseases.We studied the effect of maraviroc on TBI-induced neuroinflammation.A moderate-TBI mouse model was subjected to a controlled cortical impact device.Maraviroc or vehicle was injected intraperitoneally 1 hour after TBI and then once per day for 3 consecutive days.Western blot,immunohistochemistry,and TUNEL(terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling)analyses were performed to evaluate the molecular mechanisms of maraviroc at 3 days post-TBI.Our results suggest that maraviroc administration reduced NACHT,LRR,and PYD domains-containing protein 3 inflammasome activation,modulated microglial polarization from M1 to M2,decreased neutrophil and macrophage infiltration,and inhibited the release of inflammatory factors after TBI.Moreover,maraviroc treatment decreased the activation of neurotoxic reactive astrocytes,which,in turn,exacerbated neuronal cell death.Additionally,we confirmed the neuroprotective effect of maraviroc using the modified neurological severity score,rotarod test,Morris water maze test,and lesion volume measurements.In summary,our findings indicate that maraviroc might be a desirable pharmacotherapeutic strategy for TBI,and C-C chemokine receptor type 5 might be a promising pharmacotherapeutic target to improve recovery after TBI.展开更多
文摘目的:探讨嗜酸粒细胞活化趋化因子(eotaxin)与其相应受体CCR3的表达在慢性自发性荨麻疹发病中的作用。方法:采用酶联免疫吸附试验检测45例慢性自发性荨麻疹患者及30例正常人血清中eotaxin水平;同时用流式细胞仪分析外周血中CCR3的表达。结果:与正常对照组相比,患者组血清中eotaxin明显升高[(198.63±46.35)pg/m L vs(104.55±38.45)pg/m L];外周血CCR3表达水平显著增加[(38.24±6.87)%vs(20.37±5.40)%],差异均有统计学意义(t值分别为4.25、11.98,P值均<0.05)。结论:具有生物活性趋化因子及其受体介导的嗜酸性粒细胞的聚集、激活后释放的炎性介质在慢性自发性荨麻疹发病中起着重要作用。
基金supported by grants from the National Natural Science Foundation of China, Nos. 81930031 (to JNZ), 81720108015 (to JNZ), 81901525 (to SZ), 82101440 (to DDS), 81801234 (to YZ) and 82071389 (to GLY)the Natural Science Foundation of Tianjin, Nos. 20JCQNJC01270 (to JWW), 20JCQNJC00460 (to GLY), 18JCQNJC81000 (to HTR)+4 种基金Scientific Research Project of Tianjin Education Commission (Natural Science), No. 2018KJ052 (to ZWZ)Tianjin Health and Health Committee Science and Technology Project, No. QN20015 (to JWW)the Science & Technology Development Fund of Tianjin Education Commission for Higher Education, No. 2016YD02 (to YW)Tianjin Key Science and Technology Projects of Innovative Drugs and Medical Devices, No. 19ZXYXSY00070 (to YW)the Clinical Research Fundation of Tianjin Medical University, No. 2018kylc002 (to YW)
文摘Neuroinflammation and the NACHT,LRR,and PYD domains-containing protein 3 inflammasome play crucial roles in secondary tissue damage following an initial insult in patients with traumatic brain injury(TBI).Maraviroc,a C-C chemokine receptor type 5 antagonist,has been viewed as a new therapeutic strategy for many neuroinflammatory diseases.We studied the effect of maraviroc on TBI-induced neuroinflammation.A moderate-TBI mouse model was subjected to a controlled cortical impact device.Maraviroc or vehicle was injected intraperitoneally 1 hour after TBI and then once per day for 3 consecutive days.Western blot,immunohistochemistry,and TUNEL(terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling)analyses were performed to evaluate the molecular mechanisms of maraviroc at 3 days post-TBI.Our results suggest that maraviroc administration reduced NACHT,LRR,and PYD domains-containing protein 3 inflammasome activation,modulated microglial polarization from M1 to M2,decreased neutrophil and macrophage infiltration,and inhibited the release of inflammatory factors after TBI.Moreover,maraviroc treatment decreased the activation of neurotoxic reactive astrocytes,which,in turn,exacerbated neuronal cell death.Additionally,we confirmed the neuroprotective effect of maraviroc using the modified neurological severity score,rotarod test,Morris water maze test,and lesion volume measurements.In summary,our findings indicate that maraviroc might be a desirable pharmacotherapeutic strategy for TBI,and C-C chemokine receptor type 5 might be a promising pharmacotherapeutic target to improve recovery after TBI.
