Abstract
Plaque biofilm is the primary etiological agent of periodontal disease. Biofilm formation progresses through multiple developmental stages beginning with bacterial attachment to a surface, followed by development of microcolonies and finally detachment and dispersal from a mature biofilm as free planktonic bacteria. Tissue damage arising from inflammatory response to biofilm is one of the hallmark features of periodontal disease. A consequence of tissue damage is the release of ATP from within the cell into the extracellular space. Extracellular ATP (eATP) is an example of a danger associated molecular pattern (DAMP) employed by mammalian cells to elicit inflammatory and damage healing responses. Although, the roles of eATP as a signaling molecule in multi-cellular organisms have been relatively well studied, exogenous ATP also influences bacteria biofilm formation. Since plaque biofilms are continuously exposed to various stresses including exposure to the host damage factors such as eATP, we hypothesized that eATP, in addition to eliciting inflammation could potentially influence the biofilm lifecycle of periodontal associated bacteria. We found that eATP rather than nutritional factors or oxidative stress induced dispersal of Fusobacterium nucleatum, an organism associated with periodontal disease. eATP induced biofilm dispersal through chelating metal ions present in biofilm. Dispersed F. nucleatum biofilm, regardless of natural or induced dispersal by exogenous ATP, were more adhesive and invasive compared to planktonic or biofilm counterparts, and correspondingly activated significantly more pro-inflammatory cytokine production in infected periodontal fibroblasts. Dispersed F. nucleatum also showed higher expression of fadA, a virulence factor implicated in adhesion and invasion, compared to planktonic or biofilm bacteria. This study revealed for the first time that periodontal bacterium is capable of co-opting eATP, a host danger signaling molecule to detach from biofilms. Our results further showed that dispersed F. nucleatum possessed distinct virulence characteristics compared to their biofilm and planktonic counterparts.
Highlights
Plaque biofilm is the primary etiological agent of periodontal disease which is the main cause of tooth loss in adults (Marsh, 1994, 2003)
Given the essential role of F. nucleatum in plaque biofilm, this study aims to determine if nutritional factors, oxidative stress and Extracellular adenosine triphosphate (ATP) (eATP) modulate biofilm dispersal of F. nucleatum, and to determine if dispersed bacteria differ in its capacity to elicit inflammation compared to planktonic or biofilm forms of F. nucleatum
While subgingival plaque bacteria is the primary etiological agent of periodontitis, inappropriate host inflammatory responses mounted against plaque bacteria and their products is the main contributor to the progression of periodontal disease (Pihlstrom et al, 2005)
Summary
Plaque biofilm is the primary etiological agent of periodontal disease which is the main cause of tooth loss in adults (Marsh, 1994, 2003). Biofilm formation typically progresses through multiple eATP Induces Biofilm Dispersal developmental stages beginning with bacterial attachment to a surface, followed by development of microcolonies. A challenge in eradicating bacteria in biofilm is their increased resistance to antimicrobial agents and host defenses compared to their planktonic counterparts (Mah and O’toole, 2001). The final stage of biofilm development is the detachment of cells where bacteria disperse from a mature biofilm as free planktonic bacteria. Dispersal is an important stage in the biofilm life cycle that contributes to bacterial survival, persistence, and disease transmission (Kaplan, 2010). Dispersed Pseudomonas aeruginosa have been found to possess enhanced virulence compared to planktonic cells (Chua et al, 2014)
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