Immunological Mechanisms Underlying Chronic Pelvic Pain and Prostate Inflammation in Chronic Pelvic Pain Syndrome.
Immunological Mechanisms Underlying Chronic Pelvic Pain and Prostate Inflammation in Chronic Pelvic Pain Syndrome.
复制标题
慢性盆腔疼痛综合征患者慢性盆腔疼痛和前列腺炎症的免疫学机制。
DOI：
10.3389/fimmu.2017.00898
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发表时间：
2017
影响因子：
7.3
通讯作者：
Motrich RD
中科院分区：
文献类型：
--
作者：
Breser ML;Salazar FC;Rivero VE;Motrich RD
慢性前列腺炎/慢性盆腔疼痛综合征 (CP/CPPS) 是 50 岁以下男性最常见的泌尿系统疾病，其特征是各种类型和严重程度的疼痛和炎症症状，涉及骨盆、会阴、阴囊、直肠、睾丸、阴茎和下背部区域。在大多数患者中，在没有入侵感染因子的情况下，疼痛伴随着炎症。由于 CP/CPPS 病因学尚未完全确定，患者可用的治疗方案无论是对于医生还是患者来说都远远不能令人满意。在过去的二十年中，慢性炎症作为 CP/CPPS 的病因已被深入探讨。在这篇综述文章中，我们总结了有关 CP/CPPS 慢性盆腔疼痛和前列腺炎症的免疫机制的最新知识。从人类疾病和动物模型中获得的累积证据表明，多种因素可能以针对前列腺的自身免疫的形式引发慢性炎症，促进Th1细胞和其他不同白细胞（包括肥大细胞）的慢性前列腺募集，这可能是随后发展为慢性盆腔疼痛的主要因素。因此，局部炎症环境和炎症介质的分泌可能诱发神经敏化，导致慢性盆腔疼痛的发生。尽管科学进步令人鼓舞，但迫切需要进行更多研究来确定前列腺炎发展、肥大细胞募集到前列腺以及它们引起盆腔疼痛的精确机制之间的关系。
Chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) is the most common urologic morbidity in men younger than 50 years and is characterized by a diverse range of pain and inflammatory symptoms, both in type and severity, that involve the region of the pelvis, perineum, scrotum, rectum, testes, penis, and lower back. In most patients, pain is accompanied by inflammation in the absence of an invading infectious agent. Since CP/CPPS etiology is still not well established, available therapeutic options for patients are far from satisfactory for either physicians or patients. During the past two decades, chronic inflammation has been deeply explored as the cause of CP/CPPS. In this review article, we summarize the current knowledge regarding immunological mechanisms underlying chronic pelvic pain and prostate inflammation in CP/CPPS. Cumulative evidence obtained from both human disease and animal models indicate that several factors may trigger chronic inflammation in the form of autoimmunity against prostate, fostering chronic prostate recruitment of Th1 cells, and different other leukocytes, including mast cells, which might be the main actors in the consequent development of chronic pelvic pain. Thus, the local inflammatory milieu and the secretion of inflammatory mediators may induce neural sensitization leading to chronic pelvic pain development. Although scientific advances are encouraging, additional studies are urgently needed to establish the relationship between prostatitis development, mast cell recruitment to the prostate, and the precise mechanisms by which they would induce pelvic pain.