Department of Obstetrics and Gynecology, Medical University of Vienna, 1090 Vienna, Austria.
Molecular Diagnostics, Center for Health & Bioresources, AIT Austrian Institute of Technology Vienna, 1210 Vienna, Austria.
Int J Mol Sci. 2023 Mar 6;24(5):5022. doi: 10.3390/ijms24055022.
Endometriotic lesions are able to infiltrate surrounding tissue. This is made possible partly by an altered local and systemic immune response that helps achieve neoangiogenesis, cell proliferation and immune escape. Deep-infiltrating endometriosis (DIE) differs from other subtypes through the invasion of its lesions over 5 mm into affected tissue. Despite the invasive nature of these lesions and the wider range of symptoms they can trigger, DIE is described as a stable disease. This elicits the need for a better understanding of the underlying pathogenesis. We used the "Proseek Multiplex Inflammation I Panel" in order to simultaneously detect 92 inflammatory proteins in plasma and peritoneal fluid (PF) of controls and patients with endometriosis, as well as in particular patients with DIE, in order to gain a better insight into the systemically and locally involved immune response. Extracellular newly identified receptor for advanced gycation end-products binding protein (EN-RAGE), C-C motif Chemokine ligand 23 (CCL23), Eukaryotic translation initiation factor 4-binding protein 1 (4E-BP1) and human glial cell-line derived neurotrophic factor (hGDNF) were significantly increased in plasma of endometriosis patients compared to controls, whereas Hepatocyte Growth factor (HGF) and TNF-related apoptosis inducing ligand (TRAIL) were decreased. In PF of endometriosis patients, we found Interleukin 18 (IL-18) to be decreased, yet Interleukin 8 (IL-8) and Interleukin 6 (IL-6) to be increased. TNF-related activation-induced cytokine (TRANCE) and C-C motif Chemokine ligand 11 (CCL11) were significantly decreased in plasma, whereas C-C motif Chemokine ligand 23 (CCL23), Stem Cell Factor (SCF) and C-X-C motif chemokine 5 (CXCL5) were significantly increased in PF of patients with DIE compared to endometriosis patients without DIE. Although DIE lesions are characterized by increased angiogenetic and pro-inflammatory properties, our current study seems to support the theory that the systemic immune system does not play a major role in the pathogenesis of these lesions.
子宫内膜异位症病灶能够浸润周围组织。这在一定程度上是由于局部和全身免疫反应的改变，有助于实现新血管生成、细胞增殖和免疫逃避。深部浸润性子宫内膜异位症 (DIE) 与其他亚型不同，其病灶侵入受影响组织的深度超过 5 毫米。尽管这些病变具有侵袭性，可能引发更广泛的症状，但 DIE 被描述为一种稳定的疾病。这就需要更好地了解其潜在的发病机制。我们使用“Proseek 多重炎症 I 面板”，以便同时检测对照组和子宫内膜异位症患者以及特定的 DIE 患者的血浆和腹腔液 (PF) 中 92 种炎症蛋白，以更好地了解全身和局部参与的免疫反应。新鉴定的细胞外晚期糖基化终产物受体结合蛋白 (EN-RAGE)、C-C 基序趋化因子配体 23 (CCL23)、真核翻译起始因子 4 结合蛋白 1 (4E-BP1) 和人神经胶质细胞衍生神经营养因子 (hGDNF) 在子宫内膜异位症患者的血浆中明显高于对照组，而肝细胞生长因子 (HGF) 和肿瘤坏死因子相关凋亡诱导配体 (TRAIL) 则减少。在子宫内膜异位症患者的 PF 中，我们发现白细胞介素 18 (IL-18) 减少，而白细胞介素 8 (IL-8) 和白细胞介素 6 (IL-6) 增加。肿瘤坏死因子相关激活诱导细胞因子 (TRANCE) 和 C-C 基序趋化因子配体 11 (CCL11) 在血浆中明显减少，而 C-C 基序趋化因子配体 23 (CCL23)、干细胞因子 (SCF) 和 C-X-C 基序趋化因子 5 (CXCL5) 在 DIE 患者的 PF 中明显增加，与没有 DIE 的子宫内膜异位症患者相比。尽管 DIE 病变的特征是血管生成和促炎特性增加，但我们目前的研究似乎支持这样一种理论，即全身免疫系统在这些病变的发病机制中不起主要作用。
