Ischemia/reperfusion (I/R) injury is an inflammatory condition that is characterized by innate immunity and an adaptive immune response. This review is focused on the acute inflammatory response in I/R injury, and als...Ischemia/reperfusion (I/R) injury is an inflammatory condition that is characterized by innate immunity and an adaptive immune response. This review is focused on the acute inflammatory response in I/R injury, and also the adaptive immunological mechanisms in chronic ischemic disease that lead to increased vulnerability during acute events, in relation to the cell types that have been shown to mediate innate immunity to an adaptive immune response in I/R, specifically myocardial infarction. Novel aspects are also highlighted in respect to the mechanisms within the cardiovascular system and cardiovascular risk factors that may be involved in the inflammatory response accompanying myocardial infarction. Experimental myocardial I/R has suggested that immune cells may mediate reperfusion injury. Specifically, monocytes, macrophages, T-cells, mast cells,platelets and endothelial cells are discussed with reference to the complement cascade, toll-like receptors, cytokines, oxidative stress, renin-angiotensin system, and in reference to the microvascular system in the signaling mechanisms of I/R. Finally, the findings of the data summarized in this review are most important for possible translation into clinical cardiology practice and possible avenues for drug development.展开更多
目的探讨T、B淋巴细胞和肥大细胞在曲张大隐静脉(varicose great saphenous vein,VGSV)血管壁中的浸润变化。方法收集不同临床分期的曲张大隐静脉主干标本,采用免疫组织化学染色和甲苯胺蓝特殊染色分别检测9例曲张静脉伴有皮肤营养改变...目的探讨T、B淋巴细胞和肥大细胞在曲张大隐静脉(varicose great saphenous vein,VGSV)血管壁中的浸润变化。方法收集不同临床分期的曲张大隐静脉主干标本,采用免疫组织化学染色和甲苯胺蓝特殊染色分别检测9例曲张静脉伴有皮肤营养改变(皮肤改变组)、10例单纯曲张静脉(曲张组)和9例正常静脉组织(对照组)CD45RO、CD20及肥大细胞表达。结果T淋巴细胞、B淋巴细胞、肥大细胞计数在皮肤改变组为0.13±0.05/HP、0.05±0.05/HP、0.26±0.10/HP,曲张组为0.08±0.05/HP、0.07±0.06/HP、0.18±0.10/HP,对照组为0.13±0.06/HP、0.05±0.04/HP、0.26±0.17/HP,3组之间比较差异无显著性意义(均P>0.05)。结论下肢曲张静脉病期的变化与T、B淋巴细胞和肥大细胞血管壁的浸润无相关性。展开更多
Aim： To evaluate the immunohistopathological changes in the contralateral testis of rats after an experimental spermatic cord torsion. Methods： Male Sprague-Dawley rats of 45-50 days old were subjected to a 720°...Aim： To evaluate the immunohistopathological changes in the contralateral testis of rats after an experimental spermatic cord torsion. Methods： Male Sprague-Dawley rats of 45-50 days old were subjected to a 720° unilateral spermatic cord torsion for 10, 30 and 80 days （experimental group, E）, respectively or sham operation （control group, C）. Histopathology of the contralateral testis as well as germ cell apoptosis were studied using the Terminal Deoxynucleotidyl Transferase Biotin-dUTP Nick End Labeling （TUNEL） technique. The number of testicular lymphocytes, mast cells and macrophages, and the expression of tumor necrosis factor-α （TNF-α） and its receptor （TNFR1） in testicular cells of the contralateral testis were quantified by histochemistry and immunohistochemistry. TNF-α concentration in testicular fluid was determined by ELISA. Results： In the contralateral testis of rats from the E group, the maximal degree of damage of the germinal epithelium was seen 30 days after torsion. At this time we observed in the E group vs. the C group increases： （i） the number of testicular T-lymphocytes; （ii） the number of testicular mast cells and macrophages; （iii） the percentage of macrophages expressing TNF-α; （iv） TNF-α concentration in testicular fluid; （v） the number of apoptotic germ cells; and （vi） the number of TNFR1^＋ germ cells. Conclusion： Experimental spermatic cord torsion induces, in the contralateral testis, a focal damage of seminiferous tubules characterized by apoptosis and sloughing of germ cells. Results suggest humoral and cellular immune mediated testicular cell damage in which macrophages and mast cells seem to be involved in the induction of germ cell apoptosis through the TNF-α/TNFR1 system and in the modulation of the inflammatory process.展开更多
基金Supported by Grants from American Heart Association Post-doctoral Fellowship No. 10POST3870022 to Dr. Zuidema MYAmerican Heart Association SDG No. 110350047ANIHgrants No. RO1-HL077566 and RO1-HL085119 to Zhang C
文摘Ischemia/reperfusion (I/R) injury is an inflammatory condition that is characterized by innate immunity and an adaptive immune response. This review is focused on the acute inflammatory response in I/R injury, and also the adaptive immunological mechanisms in chronic ischemic disease that lead to increased vulnerability during acute events, in relation to the cell types that have been shown to mediate innate immunity to an adaptive immune response in I/R, specifically myocardial infarction. Novel aspects are also highlighted in respect to the mechanisms within the cardiovascular system and cardiovascular risk factors that may be involved in the inflammatory response accompanying myocardial infarction. Experimental myocardial I/R has suggested that immune cells may mediate reperfusion injury. Specifically, monocytes, macrophages, T-cells, mast cells,platelets and endothelial cells are discussed with reference to the complement cascade, toll-like receptors, cytokines, oxidative stress, renin-angiotensin system, and in reference to the microvascular system in the signaling mechanisms of I/R. Finally, the findings of the data summarized in this review are most important for possible translation into clinical cardiology practice and possible avenues for drug development.
文摘目的探讨T、B淋巴细胞和肥大细胞在曲张大隐静脉(varicose great saphenous vein,VGSV)血管壁中的浸润变化。方法收集不同临床分期的曲张大隐静脉主干标本,采用免疫组织化学染色和甲苯胺蓝特殊染色分别检测9例曲张静脉伴有皮肤营养改变(皮肤改变组)、10例单纯曲张静脉(曲张组)和9例正常静脉组织(对照组)CD45RO、CD20及肥大细胞表达。结果T淋巴细胞、B淋巴细胞、肥大细胞计数在皮肤改变组为0.13±0.05/HP、0.05±0.05/HP、0.26±0.10/HP,曲张组为0.08±0.05/HP、0.07±0.06/HP、0.18±0.10/HP,对照组为0.13±0.06/HP、0.05±0.04/HP、0.26±0.17/HP,3组之间比较差异无显著性意义(均P>0.05)。结论下肢曲张静脉病期的变化与T、B淋巴细胞和肥大细胞血管壁的浸润无相关性。
文摘Aim： To evaluate the immunohistopathological changes in the contralateral testis of rats after an experimental spermatic cord torsion. Methods： Male Sprague-Dawley rats of 45-50 days old were subjected to a 720° unilateral spermatic cord torsion for 10, 30 and 80 days （experimental group, E）, respectively or sham operation （control group, C）. Histopathology of the contralateral testis as well as germ cell apoptosis were studied using the Terminal Deoxynucleotidyl Transferase Biotin-dUTP Nick End Labeling （TUNEL） technique. The number of testicular lymphocytes, mast cells and macrophages, and the expression of tumor necrosis factor-α （TNF-α） and its receptor （TNFR1） in testicular cells of the contralateral testis were quantified by histochemistry and immunohistochemistry. TNF-α concentration in testicular fluid was determined by ELISA. Results： In the contralateral testis of rats from the E group, the maximal degree of damage of the germinal epithelium was seen 30 days after torsion. At this time we observed in the E group vs. the C group increases： （i） the number of testicular T-lymphocytes; （ii） the number of testicular mast cells and macrophages; （iii） the percentage of macrophages expressing TNF-α; （iv） TNF-α concentration in testicular fluid; （v） the number of apoptotic germ cells; and （vi） the number of TNFR1^＋ germ cells. Conclusion： Experimental spermatic cord torsion induces, in the contralateral testis, a focal damage of seminiferous tubules characterized by apoptosis and sloughing of germ cells. Results suggest humoral and cellular immune mediated testicular cell damage in which macrophages and mast cells seem to be involved in the induction of germ cell apoptosis through the TNF-α/TNFR1 system and in the modulation of the inflammatory process.
