Chung Hyo-Yeoung, Kim Jung-Hyun, Han Ik-Hwan, Ryu Jae-Sook
Department of Environmental Biology and Medical Parasitology, Hanyang University College of Medicine, Seoul 04763, Korea.
Department of Biomedical Science, Hanyang University Graduate School of Biomedical Science and Engineering, Seoul 04763, Korea.
Korean J Parasitol. 2020 Jun;58(3):217-227. doi: 10.3347/kjp.2020.58.3.217. Epub 2020 Jun 26.
Trichomonas vaginalis causes inflammation of the prostate and has been detected in tissues of prostate cancers (PCa), prostatitis and benign prostatic hyperplasia. Obesity is a risk factor for PCa and causes a chronic subclinical inflammation. This chronic inflammation further exacerbates adipose tissue inflammation as results of migration and activation of macrophages. Macrophages are the most abundant immune cells in the PCa microenvironment. M2 macrophages, known as Tumor-Associated Macrophages, are involved in increasing cancer malignancy. In this study, conditioned medium (TCM) of PCa cells infected with live trichomonads contained chemokines that stimulated migration of the mouse preadipocytes (3T3-L1 cells). Conditioned medium of adipocytes incubated with TCM (ATCM) contained Th2 cytokines (IL-4, IL-13). Macrophage migration was stimulated by ATCM. In macrophages treated with ATCM, expression of M2 markers increased, while M1 markers decreased. Therefore, it is suggested that ATCM induces polarization of M0 to M2 macrophages. In addition, conditioned medium from the macrophages incubated with ATCM stimulates the proliferation and invasiveness of PCa. Our findings suggest that interaction between inflamed PCa treated with T. vaginalis and adipocytes causes M2 macrophage polarization, so contributing to the progression of PCa.
阴道毛滴虫可引发前列腺炎症,且已在前列腺癌(PCa)、前列腺炎及良性前列腺增生的组织中检测到。肥胖是PCa的一个风险因素,并会引发慢性亚临床炎症。这种慢性炎症会因巨噬细胞的迁移和激活而进一步加剧脂肪组织炎症。巨噬细胞是PCa微环境中最为丰富的免疫细胞。M2巨噬细胞,即肿瘤相关巨噬细胞,参与增加癌症的恶性程度。在本研究中,感染活滴虫的PCa细胞的条件培养基(TCM)含有刺激小鼠前脂肪细胞(3T3-L1细胞)迁移的趋化因子。与TCM共同孵育的脂肪细胞的条件培养基(ATCM)含有Th2细胞因子(IL-4、IL-13)。ATCM刺激巨噬细胞迁移。在用ATCM处理的巨噬细胞中,M2标志物的表达增加,而M1标志物的表达减少。因此,提示ATCM可诱导M0巨噬细胞向M2巨噬细胞极化。此外,与ATCM共同孵育的巨噬细胞的条件培养基可刺激PCa的增殖和侵袭性。我们的研究结果表明,经阴道毛滴虫处理的炎症性PCa与脂肪细胞之间的相互作用会导致M2巨噬细胞极化,从而促进PCa的进展。