Dmowski W P, Gebel H, Braun D P
Rush Medical College and Institute for the Study and Treatment of Endometriosis, Webster, Chicago, IL 60614, USA.
Hum Reprod Update. 1998 Sep-Oct;4(5):696-701. doi: 10.1093/humupd/4.5.696.
Ectopic dissemination of endometrial cells and their subsequent implantation are the mechanisms involved in the development of endometriosis. While the process of dissemination appears to be a phenomenon common to all women, it is unknown what facilitates or prevents ectopic implantation of misplaced endometrial cells. Prior studies by our group and others suggest that cell-mediated immunity in patients with endometriosis is decreased. The present studies evaluated (i) peripheral blood monocyte (PBM) and peritoneal macrophage (PM) mediated cytolysis of autologous eutopic and ectopic endometrial cells and (ii) programmed cell death (apoptosis) in the eutopic and ectopic endometrium. PBM-mediated cytolysis was (mean+/-SD) 23.1+/-13% for the eutopic and 7.8+/-% for the ectopic endometrium (P < 0.004), while the corresponding percentages for PM-mediated cytolysis were 5.4+/-7 and 0.3+/-1 respectively (P < 0.04). This indicates that PBM are much more effective than PM in inducing cytolysis of both eutopic and ectopic endometrium and that ectopic endometrial cells are significantly more resistant to both PBM- and PM-mediated cytolysis. The apoptosis was significantly decreased in the eutopic endometrium of women with endometriosis as compared to fertile controls (0.375+/-0.17 versus 1.57+/-0.3, P < 0.0001). Furthermore, in matched samples apoptosis was significantly lower in the ectopic (0.149+/-0.075) than eutopic (0.375+/-0.17) endometrium (P < 0.001). We conclude from these studies that the decrease in the capacity of monocytes to mediate cytolysis of the misplaced endometrial cells in the peritoneal locations and an increased resistance of these cells to apoptosis are fundamental to the aetiology and/or pathophysiology of endometriosis.
子宫内膜细胞的异位播散及其随后的着床是子宫内膜异位症发生发展的机制。虽然播散过程似乎是所有女性共有的现象，但尚不清楚是什么促进或阻止了异位的子宫内膜细胞着床。我们团队和其他团队之前的研究表明，子宫内膜异位症患者的细胞介导免疫功能下降。本研究评估了：（i）外周血单核细胞（PBM）和腹腔巨噬细胞（PM）介导的自体在位和异位子宫内膜细胞的细胞溶解作用，以及（ii）在位和异位子宫内膜中的程序性细胞死亡（凋亡）。PBM介导的在位子宫内膜细胞溶解率（均值±标准差）为23.1±13%，异位子宫内膜细胞溶解率为7.8±%（P<0.004），而PM介导的细胞溶解率相应百分比分别为5.4±7和0.3±1（P<0.04）。这表明，PBM在诱导在位和异位子宫内膜细胞溶解方面比PM有效得多，并且异位子宫内膜细胞对PBM和PM介导的细胞溶解均具有显著更高的抗性。与可育对照相比，子宫内膜异位症女性在位子宫内膜中的凋亡显著减少（0.375±0.17对1.57±0.3，P<0.0001）。此外，在配对样本中，异位子宫内膜（0.149±0.075）中的凋亡显著低于在位子宫内膜（0.375±0.17）（P<0.001）。我们从这些研究中得出结论，单核细胞介导腹腔内异位子宫内膜细胞溶解的能力下降以及这些细胞对凋亡的抗性增加是子宫内膜异位症病因学和/或病理生理学的基础。
