Tobacco enhances pathogenicity of Filifactor alocis leading to Periodontitis

Filifactor alocis was grown in vitro and cigarette smoke extract-responsive genes determined by RNAseq. Mice were exposed, or not, to mainstream 1R6F research cigarette smoke and infected with F. alocis, or not, in an acute ligature model of periodontitis. Key clinical, infectious, and immune data were collected.

Results

• In culture, F. alocis growth was unaffected by smoke conditioning and only a small number of genes were specifically regulated by smoke exposure.
• Reduced murine mass, differences in F. alocis-cognizant antibody production, and altered immune profiles as well as altered alveolar bone loss were all attributable to smoke exposure and/or F. alocis infection in vivo.

Thus, F. alocis is well-adapted to tobacco-rich conditions and its pathogenesis is enhanced by tobacco smoke exposure. A smoke-exposed ligature model of periodontitis shows promise as a tool with which to further unravel mechanisms underlying tobacco-enhanced, bacteria-induced disease.

Reference:

Iskander, M. M. Z., Lamont, G. J., Tan, J., Pisano, M., Uriarte, S. M., & Scott, D. A. (2022). Tobacco smoke exacerbates Filifactor alocis pathogenicity. Journal of Clinical Periodontology, 1– 10. https://doi.org/10.1111/jcpe.13729

Keywords:

Tobacco, enhances, pathogenicity, Filifactor, alocis, Periodontitis, Journal of Clinical Periodontology, Mina M. Z. Iskander, Gwyneth J. Lamont, Jinlian Tan, Michele Pisano,Silvia M. Uriarte, David A. Scott