Porphyromonas gingivalis infection of esophageal cancer cells induces M2 macrophage polarization and promotes esophageal cancer progression

Acta Universitatis Medicinalis Anhui 2023 05 v.58 780-787     font:big middle small

Found programs:

Authors:Guo Jingyi; Yuan Xiang; Shi Linlin; Zhang Xiusen; Kong Jinyu; Zhang Dingyu; Gao Shegan

Keywords:esophageal squamous cell carcinoma;cytokines;THP-1 cells;macrophages

DOI:10.19405/j.cnki.issn1000-1492.2023.05.013

〔Abstract〕 Objective To investigate the effect of Porphyromonas gingivallis(Pg) infection of esophageal cancer cells on the polarization of tumor associated macrophages(TAMS) and functional changes.Methods The secretion of tumor-related cytokines in the supernatant of Pg infected and uninfected esophageal squamous cell carcinoma(ESCC) cells was detected by ELISA.A co-culture model of ESCC cells and macrophages in vitro was established,and the changes of TAMs surface markers were detected by qPCR,cellular immunofluorescence and flow cytometry.Cytokines secreted by TAMs after co-culture were detected by ELISA.ESCC cells were cultured using conditioned medium of co-cultured TAMS,and the effects of TAMs on the proliferation,migration and invasion of esophageal cancer cells were evaluated by CCK-8,Wound-healing assay and Transwell assay.Results The expression quantity of IL-6 and IL-10 of Pg-infected ESCC cells increased(P<0.01).The contents of CD 163 and CD206 on the surface of TAMs co-cultured with Pg-infected ESCC cells increased(P<0.001).The cytokines IL-6 and IL-10 secreted by TAMs co-cultured with Pg-infected ESCC cells relatively increased(P<0.01).TAMs co-cultured with Pginfected ESCC cells were able to enhance ESCC cells proliferation,migration and invasion(all P<0.05).Conclusion Pg infection of ESCC cells can induce the secretion of cytokines,remodel TAMs to polarize toward the M2-type immunosuppressive phenotype,thereby promoting the malignant biological behavior of ESCC cells.This study provides data support for the etiology of esophageal cancer and potential target molecules for clinical immunotherapy targeting TAMs.