Abstract
BackgroundTo assess the effects of Epstein–Barr virus (EBV) and human papillomavirus (HPV) infection on the tumor microenvironment, we examined the relationship between viral infection status, macrophage migration inhibitory factor (MIF), and tumor-associated macrophages in nasopharyngeal carcinoma (NPC).MethodsA tissue microarray containing 150 cores from 90 patients with NPC and six with chronic inflammation was used. EBV and HPV status were detected using in situ hybridization with commercial EBER1 and HPV16/18 probes. Immunofluorescence double staining of MIF, pan-macrophage marker CD68, M1 macrophage marker CD11c, and M2 macrophage marker CD163 were analyzed using the same tissue microarray. The levels of these markers between NPC and inflammation cases and between tumor nests and stroma were compared. Correlations among these markers were analyzed.ResultsWe found EBER1(+) cases in 90% of NPC patients, including 10% EBV/HPV co-infection. M1 macrophages mainly infiltrated the tumor nest, while M2 macrophages infiltrated the tumor stroma. We found a significant positive correlation between EBER1 levels and MIF levels in tumor nests and a significant positive correlation between HPV16/18 and CD11c(+) cell levels in NPC tissues.ConclusionsIt is suggested that MIF is associated with EBV, and M1 macrophage infiltration is affected by HPV status in NPC.
Highlights
To assess the effects of Epstein–Barr virus (EBV) and human papillomavirus (HPV) infection on the tumor microenvironment, we examined the relationship between viral infection status, macrophage migration inhibitory factor (MIF), and tumor-associated macrophages in nasopharyngeal carcinoma (NPC)
EBER1 and HPV16/18 infection status in NPC and inflammation cases After in situ hybridization (ISH), 79 NPC cases and five control inflammation cases were available in TMA_NPC1504, and 12 cases were lost during the ISH procedure
MIF, CD68, CD11c, and CD163 scores in inflammation and NPC tissues To validate the levels of these markers in inflammation and NPC tissues, MIF and CD68 were stained in one tissue microarray slide, and CD11c and CD163 in another tissue microarray slide, using immunofluorescence double staining
Summary
To assess the effects of Epstein–Barr virus (EBV) and human papillomavirus (HPV) infection on the tumor microenvironment, we examined the relationship between viral infection status, macrophage migration inhibitory factor (MIF), and tumor-associated macrophages in nasopharyngeal carcinoma (NPC). Nasopharyngeal carcinoma (NPC) is a malignant epithelial tumor that originates from the nasopharyngeal mucosal lining. It is rare worldwide; prevalent in southern China and Southern Asia [1]. EBV infection is considered the most important etiological factor of NPC [4] and is reported to change the tumor microenvironment to benefit itself, immune evasion [5]. Despite being an important component of the tumor microenvironment, the relationship among tumor-associated macrophages (TAMs), EBV, and HPV infection remains unknown in NPC
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