Aggregatibacter actinomycetemcomitans immune response affect rat’s neurons and microglias.

Objectives: Periodontitis and Alzheimer's disease (AD) are prevalent diseases in elderly population. Recently, it has been proposed that the inflammatory response caused by pathogenic bacteria in individuals affected by periodontitis could predispose to neuroinflammatory disease. Aggregatibacter actinomycetemcomitans has been associated with the most severe grades of periodontitis and, according to the antigenicity of lipopolysaccharide (LPS), different serotypes have been described with differential immunogenicity and virulence. Aim: to determine the response of cultures enriched in neurons, stimulated with purified LPS of serotypes a, b or c of A. actinomycemtcomitans.
Methods: From 3-4 days old newborn Sprague-Dawley rats were obtained neuron-enriched and microglia cultures that were stimulated with the different serotypes of A. actinomycetemcomitans. The expression or secretion levels of inflammatory cytokines were quantified by qPCR or ELISA. Subsequently, the neuronal morphology was evaluated by immunofluorescence and the Sholl analysis was performed to determine the extension of the neurites.
Results: Neuron-enriched and microglia cultures stimulated with purified LPS of serotype b of A. actinomycetecomitams produced the highest levels of cytokines and Amyloid β₄₂, and showed changes in neuronal morphology compared with the same cells stimulated with serotypes a, c or non induced.
Conclusions: The LPS of A. actinomycetemcomitans triggers inflammatory responses that affect brain cells. These results suggest that brain infiltration of LPS could induce a microglial M1 response that affect neuronal morphology and could be associated with neuroinflammation.