Porphyromonas Gingivalis Promotes Nuclear Membrane Atypia Of Gingival Epithelial Cells

Nuclear membrane atypia is usually closely related to genetic and epigenetic abnormalities in tumor cells. However, we found that persistent infection of gingival epithelial cells by Porphyromonas gingivalis (P. gingivalis) could enhance nuclear membrane atypia. We established an infection model of P. gingivalis persistently infecting gingival epithelial cell line (EPI4) for one month. Nuclear membrane atypia was evaluated by transmission electron microscopy and immunofluorescence. Transcriptional profiling combined with ATAC-seq technology was used to analyze epigenetic changes and screen potential key genes. Nuclear membrane atypia in gingival epithelial cells gradually increased with the duration of P. gingivalis infection. There were significant changes in heterochromatin localization, cell differentiation related genes and tumor related genes. The activated TRIM4 protein degraded Lamin B protein through ubiquitination, disrupting the physiological state of the nuclear membrane and promoting nuclear membrane atypia. This study evaluated the changes in nuclear membrane atypia and preliminarily explored the impact of persistent P. gingivalis infection on the epigenetic level of host cells. It proposed that the ubiquitination and degradation of Lamin B protein by TRIM4 might be an important mechanism in this process. This study provides new insights into the pathogenic mechanism and adverse outcomes of periodontitis.