Circulating inflammatory markers in cervical cancer patients and healthy controls
Circulating inflammatory markers in cervical cancer patients and healthy controls
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DOI：
10.1080/1547691x.2020.1755397
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发表时间：
2020-01-01
影响因子：
3.3
通讯作者：
Vaitkiene, Daiva
中科院分区：
文献类型：
--
作者：
Vitkauskaite, Agne;Urboniene, Daiva;Vaitkiene, Daiva
越来越多的证据表明，宿主炎症反应在癌症的发生和发展中起着重要作用。有一些数据表明，癌症不仅与病变部位的炎症有关，而且与宿主整体全身免疫反应的失调有关。就宫颈癌而言，炎症是与该疾病的发生、进展和潜在转移相关的重要因素。人类乳头状瘤病毒（HPV）是一种已知的CC病原体，可能由吸烟引起，目前尚不清楚宿主对HPV反应的潜在改变。特别是，HPV感染引起的炎症如何影响CC发病率/严重程度仍有待确定。在这项前瞻性研究中，使用Multiplex和ELISA检测来评估血清中10种细胞因子的水平。样本为43例CC患者和60例健康（NILM）对照组的血清。评估了所有结果与宿主HPV及其吸烟状况的关系。结果表明，与健康的NILM对照组相比，CC （HPV+）患者血清sTREM-1、TNF - α、IFN β、IL-1 β和IL-6水平显著升高。IL-10和IL-2水平也有类似的趋势。在两组中，吸烟者和从不吸烟者之间的细胞因子水平差异并不显著。本研究结果支持全身性炎症在CC病理生理中的假设作用。
There is increasing evidence that host inflammatory responses play an important role in the development and progression of cancers. There are some data that cancer is associated not only with inflammation at the site of the lesion, but also with dysregulations of the host overall systemic immune response. In the case of cervical cancer, inflammation is an important factor associated with the development, progression, and potential metastasis of the disease. What is unclear still in the potential for modifications of host responses to human papillomaviruses (HPV) - a known causative agent of CC, that could be induced by cigarette smoking. In particular, it remains to be determined how the inflammation induced by HPV infection could impact on CC incidence/severity. In this prospective study, serum levels of 10 cytokines were evaluated using Multiplex and ELISA assays. The samples were the sera of 43 CC patients and 60 healthy (NILM) controls. All outcomes were evaluated in relation to host HPV and to their smoking status. The results in indicated that serum sTREM-1, TNF alpha, IFN beta, IL-1 beta, and IL-6 levels were significantly increased in CC (HPV+) patients compared to healthy NILM controls. A similar trend was observed for IL-10 and IL-2 levels. Within the two groups, differences in cytokine levels between smokers and never smokers were not remarkable. The findings here support the hypothesized role of systemic inflammation in the pathophysiology of CC.