IADR Abstract Archives
Distinct Immune Responses Triggered by Aggregatibacter actinomycetemcomitans Serotypes During Experimental Periodontitis
Objectives: Aggregatibacter actinomycetemcomitans expresses a number of virulence factors that may contribute to the pathogenesis of periodontitis. Similarly to other periodonto-pathogens, A. actinomycetemcomitans can synthesize LPS, which stimulates a wide range of host immunological responses that may have important pathological consequences. Based on the antigenicity of the O-polysaccharide component of the LPS, different A. actinomycetemcomitans serotypes have been described. Among them, serotype b has demonstrated a stronger capacity to trigger Th1 and Th17-related cytokine and chemokine production on immune cells. With a murine model of experimental periodontitis, this investigation aimed to analyse the pattern of immune response triggered by the different serotypes of A. actinomycetemcomitans within experimental periodontal lesions.
Methods: Balb/c mice were orally infected with the different serotypes of A. actinomycetemcomitans or their purified LPS. Bacterial infection and alveolar bone resorption were analyzed using qPCR, scanning-electron-microscopy, and micro-CT. The expression levels for the cytokines IL-1β, IL-6, IL-12, IL-17, IL-23, IFN-γ, and TNF-α, the CC-chemokines CCL2, CCL5, and CCL20, the CC-chemokine receptors CCR2, CCR5, CCR6, CCR7, as well as the pro-bone-resorptive factor RANKL, were quantified by qPCR.
Results: Periodontal infection with the serotype b of A. actinomycetemcomitans induced higher alveolar bone resorption and expression of cytokines biased towards a Th1 and Th17-pattern of immune response compared with the other serotypes. Similarly, higher expression levels of RANKL were detected in serotype b-induced periodontal lesions, and these increased levels of RANKL positively correlated with the higher levels of cytokines. In addition, serotype b induced greater levels of Th1 and Th17-related CCLs and CCRs than the others.
Conclusions: These results demonstrate that periodontal lesions induced with different serotypes of A. actinomycetemcomitans elicited distinct alveolar bone resorption and immune response. In particular, serotype b was more pathogenic than the others and induced stronger Th1 and Th17-pattern of immune response during experimental periodontitis.
Methods: Balb/c mice were orally infected with the different serotypes of A. actinomycetemcomitans or their purified LPS. Bacterial infection and alveolar bone resorption were analyzed using qPCR, scanning-electron-microscopy, and micro-CT. The expression levels for the cytokines IL-1β, IL-6, IL-12, IL-17, IL-23, IFN-γ, and TNF-α, the CC-chemokines CCL2, CCL5, and CCL20, the CC-chemokine receptors CCR2, CCR5, CCR6, CCR7, as well as the pro-bone-resorptive factor RANKL, were quantified by qPCR.
Results: Periodontal infection with the serotype b of A. actinomycetemcomitans induced higher alveolar bone resorption and expression of cytokines biased towards a Th1 and Th17-pattern of immune response compared with the other serotypes. Similarly, higher expression levels of RANKL were detected in serotype b-induced periodontal lesions, and these increased levels of RANKL positively correlated with the higher levels of cytokines. In addition, serotype b induced greater levels of Th1 and Th17-related CCLs and CCRs than the others.
Conclusions: These results demonstrate that periodontal lesions induced with different serotypes of A. actinomycetemcomitans elicited distinct alveolar bone resorption and immune response. In particular, serotype b was more pathogenic than the others and induced stronger Th1 and Th17-pattern of immune response during experimental periodontitis.