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Inhibition of LPS‑induced NLRP3 inflammasome activation by stem cell‑conditioned culture media in human gingival epithelial cells

  • Authors:
    • Hong Li
    • Licong Sun
    • Yuesen Wang
  • View Affiliations

  • Published online on: April 5, 2023     https://doi.org/10.3892/mmr.2023.12993
  • Article Number: 106
  • Copyright: © Li et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Interleukin (IL)‑1β is a pathogenic factor associated with the destruction of periodontal tissue in periodontitis. IL‑1β processing is regulated by cytosolic machinery known as the inflammasome. Porphyromonas gingivalis infection and lipopolysaccharide (LPS) have an important role in the destruction of periodontal tissue in periodontitis. P. gingivalis infection and LPS have been reported to activate the NOD‑like receptor family pyrin domain‑containing protein 3 (NLRP3) inflammasome in human oral cells. Stem cell therapy exhibits anti‑inflammatory effects and stem cell‑conditioned culture media (SCM) shows similar beneficial effects. The present study tested the hypothesis that SCM inhibits activation of the inflammasome and protects human gingival epithelial cells (GECs) against LPS‑induced inflammatory damage. Human GECs were treated with or without LPS plus SCM or control cell media. NLPR3 inflammasome components and inflammatory factors were measured by western blotting and immunofluorescence. The present study revealed that LPS induced an increase in the expression of inflammasome components, NLRP3, apoptosis‑associated speck‑like protein containing a caspase recruitment domain (ASC) and caspase‑1. Co‑immunoprecipitation revealed increased binding of NLRP3 and ASC, and immunofluorescence showed an increased co‑localization of ASC and caspase‑1, suggesting that LPS stimulated assembly of the NLRP3 inflammasome. SCM inhibited the overexpression and assembly of NLRP3 inflammasome components induced by LPS. Furthermore, SCM blocked the increase in IL‑1β production induced by LPS and inhibited the translocation of the inflammatory factor, NF‑κB, into the nuclei. Consequently, SCM protected cells against LPS‑induced damage, as suggested by the recovery of disturbed E‑cadherin staining pattern, which indicates a disruption in epithelial integrity. In conclusion, treatment with SCM may attenuate LPS‑induced inflammatory damage in human GECs via inhibition of NLRP3 inflammasome activation, suggesting a potential therapeutic use for SCM.
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May-2023
Volume 27 Issue 5

Print ISSN: 1791-2997
Online ISSN:1791-3004

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Spandidos Publications style
Li H, Sun L and Wang Y: Inhibition of LPS‑induced NLRP3 inflammasome activation by stem cell‑conditioned culture media in human gingival epithelial cells. Mol Med Rep 27: 106, 2023
APA
Li, H., Sun, L., & Wang, Y. (2023). Inhibition of LPS‑induced NLRP3 inflammasome activation by stem cell‑conditioned culture media in human gingival epithelial cells. Molecular Medicine Reports, 27, 106. https://doi.org/10.3892/mmr.2023.12993
MLA
Li, H., Sun, L., Wang, Y."Inhibition of LPS‑induced NLRP3 inflammasome activation by stem cell‑conditioned culture media in human gingival epithelial cells". Molecular Medicine Reports 27.5 (2023): 106.
Chicago
Li, H., Sun, L., Wang, Y."Inhibition of LPS‑induced NLRP3 inflammasome activation by stem cell‑conditioned culture media in human gingival epithelial cells". Molecular Medicine Reports 27, no. 5 (2023): 106. https://doi.org/10.3892/mmr.2023.12993