1121 PGRP-S role in Jurkat apoptosis induced by Fusobacterium nucleatum

Friday, March 23, 2012: 3:30 p.m. - 4:45 p.m.
Presentation Type: Poster Session
K. EVANS1, M. RAPOZO-HILO2, Y. RAVANDOUST1, D. FRASER1, C. HOOVER3, and T. HUYNH4, 1University of California - San Francisco, San Francisco, CA, 2Prevent. & Restor. Dental Sciences, University of California - San Francisco, San Francisco, CA, 3University of California - San Francisco, Forestville, CA, 4School of Denitstry, University of California - San Francisco, San Francisco, CA
Objective: Fusobacterium nucleatum (Fn), a gram-negative oral anaerobe, has been implicated in the pathogenesis of periodontal and endodontic infections. We have shown that Fn can induce apoptosis in immune cells (Jewett 2000), and it appears that aggregation of immune cells and upregulation of death ligands play a significant role (Huynh 2011, Fraser 2010).  Peptidoglycan recognition proteins (PGRP-S) are responsible for detecting bacteria-derived peptidoglycans and for target recognition and induced death ligand mediated cell apoptosis (Sashchenko 2007).  The purpose of this study was to determine if PGRP-S has a direct role in Fn induced apoptosis in Jurkat T cells.

Method: After Jurkats were co-cultured with Fn for four hours, we assessed the expression of PGRP-S on Jurkats via flow cytometry (MoFlo Systems).  After co-culturing Fn with Jurkats overnight with monoclonal antibodies to PGRP-S, the levels of Jurkat apoptosis was assessed via caspase assay according to manufacturer instructions (Promega Caspase-Glo 3/7 Assay Kit).  ANOVA with post-hoc Tukey’s test was used for statistical analysis at p<0.05.

Result: A significant increase in PGRP-S expression was found on Jurkat-cells upon co-culture with Fn.  There was a significant dose dependent decrease in Jurkat-cell apoptosis upon co-culture with Fn in the presence of monoclonal anti-PGRP-S antibodies. 

Conclusion: The results indicate that PGRP-S has a direct role in Fusobacterium nucleatum’s ability to induce apoptotic cell death in Jurkat T cells.  Further studies are needed to elucidate the signaling pathway involved in this process.


This abstract is based on research that was funded entirely or partially by an outside source: NIDCR-5K08DE016872-03, COHORT-T32-DE007306-14

Keywords: Apoptosis, Bacterial, Endodontics, Periodontal disease and Pulpal disease