Department of Pathology, Tohoku University, Graduate School of Medicine, Sendai, Miyagi, 980-8575, Japan; Department of Surgical Oncology, Ningxia Medical University, Yinchuan, Ningxia, 750021, People's Republic of China; Department of Breast Surgery, Ningxia People's Hospital, Yinchuan, Ningxia, 750021, People's Republic of China.
Department of Surgical Oncology, Ningxia Medical University, Yinchuan, Ningxia, 750021, People's Republic of China; Department of Breast Surgery, Ningxia People's Hospital, Yinchuan, Ningxia, 750021, People's Republic of China.
Hum Pathol. 2014 Mar;45(3):606-10. doi: 10.1016/j.humpath.2013.06.025. Epub 2013 Nov 7.
Plasma cell mastitis (PCM) is one of the most frequently encountered inflammatory diseases of the nonlactating breast. Histologically, PCM is characterized by infiltration of relatively abundant plasma cells into the mammary ducts. Its pathogenesis has remained unknown. In this study, we immunolocalized intercellular adhesion molecule (ICAM) 1 and 2 and E-selectin, all of which play pivotal roles in the inflammatory process, in 35 cases of PCM. We then compared the results with those of non-PCM and nonpathologic breast tissue. In the ductal epithelium, ICAM-1 immunoreactivity was significantly more pronounced in PCM than in non-PCM (P = .045). Both ICAM-1 (P < .001) and ICAM-2 (P = .001) were significantly more pronounced in PCM than in nonpathologic breast tissue. However, no significant differences in ICAM-2 and E-selectin immunoreactivity were detected between ductal epithelium of PCM and non-PCM. ICAM-1, but not ICAM-2 or E-selectin, demonstrated significantly higher immunoreactivity in endothelial cells of PCM than in nonpathologic breast (P < .001). These results all suggest that ICAM-1 in both ductal epithelium and endothelium plays important roles in the inflammatory process of PCM, possibly through margination, extravasation, and attachment of plasma cells and lymphocytes, which may result in continuous inflammatory cell homing to ductal epithelial cells.
浆细胞性乳腺炎(PCM)是哺乳期外乳腺最常见的炎症性疾病之一。组织学上,PCM 的特征是相对丰富的浆细胞浸润乳腺导管。其发病机制尚不清楚。在这项研究中,我们免疫定位了细胞间黏附分子(ICAM)1 和 2 以及 E-选择素,这些分子在炎症过程中都起着关键作用,在 35 例 PCM 中进行了研究。然后,我们将结果与非 PCM 和非病变乳腺组织进行了比较。在导管上皮中,PCM 中 ICAM-1 的免疫反应性明显强于非 PCM(P =.045)。PCM 中 ICAM-1(P <.001)和 ICAM-2(P =.001)的表达均明显强于非病变乳腺组织。然而,PCM 和非 PCM 导管上皮中 ICAM-2 和 E-选择素的免疫反应性没有显著差异。ICAM-1,但不是 ICAM-2 或 E-选择素,在 PCM 的内皮细胞中的免疫反应性明显高于非病变乳腺组织(P <.001)。这些结果均表明,ICAM-1 在导管上皮和内皮细胞中均在 PCM 的炎症过程中发挥重要作用,可能通过边缘、渗出和浆细胞和淋巴细胞的附着,导致炎症细胞持续向导管上皮细胞归巢。