Background A major cause of chronic inflammatory periodontal diseases is Porphyromonas gingivalis (P. gingivalis), a non-motile, gram-negative, rod-shaped, anaerobic bacterium. Within gingival tissue, both macrophages and fibroblasts participate in the immune response to foreign entities by releasing cytokines and expressing molecules to recruit and activate lymphocytes. However, the contribution of gingival macrophages and fibroblasts to the immune response to P. gingivalis infection is not fully known. Methods The AMJ2-C8 cell line (AM cells), a mouse alveolar macrophage cell line, and ESK-1 cells, a mouse gingival fibroblast cell line made in our laboratory, were treated with lipopolysaccharide (LPS) from either P. gingivalis or Escherichia coli (E. coli). The expression of immune response molecules was quantified by real-time PCR and enzyme-linked immunoassay. Results AM and ESK-1 cells responded differently to P. gingivalis and E. coli LPS stimulation. The ESK-1 gingival fibroblast cell line was more responsive to E. coli LPS stimulation as seen by elevated levels of interleukin (IL)-6, inducible nitric oxide (iNOS), and monocyte chemotactic protein-1 (MCP-1) expression relative to stimulation by P. gingivalis LPS. Conversely, the AM macrophage cell line was more responsive to P. gingivalis LPS stimulation, particularly for interleukin IL-1β, IL-6, and MCP-1, relative to stimulation by E. coli LPS. Conclusion These findings demonstrate that E. coli LPS induces a stronger cytokine/chemokine response in gingival fibroblasts, while P. gingivalis LPS induces a stronger response in macrophages.
Background and Objective Porphyromonas gingivalis infection is strongly associated with periodontitis. Although P. gingivalis is known to elicit a strong inflammatory response, details of that remain fragmentary. To understand the local response to P. gingivalis, primary cell lines derived from mouse gingival tissues were exposed to P. gingivalis or E. coli lipopolysaccharide (LPS), and cytokine production for interleukin-6 (IL-6) and tumor necrosis factor-α (TNFα were measured. CCL25 gene expression was measured by real-time PCR. Cells stimulated with combinations of IL-6, soluble IL-6 receptor (sIL-6R), and/or soluble gp130 (sgp130) were assayed for CCL2 and TNFα secretion. Methods Primary cell lines were generated from mouse gingival tissues. Enzyme-linked assays were used to determine cytokine levels, and real-time PCR was used to quantify CCL25 gene expression. Results Exposure to P. gingivalis but not E. coli LPS resulted in significantly elevated levels of both IL-6 and TNFα, and P. gingivalis LPS-stimulation also upregulated CCL25 gene expression. In one of three experiments, IL-6 induced CCL2 secretion, whereas IL-6 with sIL-6R induced CCL2 secretion in all three experiments, suggesting that both direct IL-6 signaling and IL-6 trans-signaling may be involved. However, because sgp130 did not inhibit trans-signaling, and because direct stimulation of gingival cells with sgp130 resulted in CCL2 secretion, the possibility exists that sgp130 forms binary complexes with soluble IL-6R that promote direct IL-6 stimulation. Conclusion These findings define a pathway in which exposure of gingival cells to P. gingivalis induces the release of IL-6 and TNFα; IL-6 in turn induces CCL2 secretion.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.