Can angiotensin II affect the inflammatory response of human dental pulp cells in vitro?

Abstract Dental pulp fibroblasts respond to various stimuli, including microbial agents, endodontic materials, restorative procedures, pulp protection treatments, and inflammatory molecules. Its inflammatory response to injury involves a complex set of mechanisms that have been increasingly studied for their roles in this intricate biological process. Among these mechanisms is angiotensin II (ANG-II), the involvement of which in inflammation has been shown in several pathological conditions via its local generation and action. Objective This study aimed to evaluate the capacity of fibroblasts from permanent and deciduous dental pulp to express inflammatory mediators when exposed to bacterial and inflammatory antigens. It also sought to assess the presence of components of the renin-angiotensin system (RAS) and the potential modulatory role of ANG-II in this response. Methodology Fibroblasts were cultured from the pulp of permanent and deciduous teeth obtained from three adult and four pediatric donors with informed consent. Cells were stimulated with Porphyromonas gingivalis and Escherichia coli lipopolysaccharides (LPS) either alone or in combination with ANG-II and, in some cases, with IL-1β. Gene expression of RAS components and various inflammatory mediators was analyzed by qRT-PCR. ANG-II receptor expression was quantified by flow cytometry. Results The results showed that both bacterial antigens and IL-1β significantly upregulated the expression of genes encoding key inflammatory mediators. However, ANG-II, either alone or in combination with other antigens, failed to alter the expression levels of these mediators. Conclusion These findings clearly show that ANG-II has no influence on the expression of inflammatory mediators by human dental pulp fibroblasts under the tested conditions.