Lipopolysaccharide fromPorphyromonas gingivalispromotes autophagy of human gingival fibroblasts through the PI3K/Akt/mTOR signaling pathway

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Abstract

Aims:

Lipopolysaccharide (LPS) is a major component of cell wall in gram-negative bacteria and has been proved to be a predominant pathogenic factor in periodontitis. Porphyromonas gingivalis (P.g) was abundant in patients with periodontitis and was associated with patient clinic-pathological characteristics. Furthermore, autophagy is a potential mechanism in inflammatory disease. In this study, we hypothesized that LPS from P.g may affect the physiological functions of human gingival fibroblasts (HGFs) through activating cellular autophagy. However, it remains unclear what molecular basis related to LPS-induced autophagy in HGFs.

Main methods:

Here, we initially addressed the contribution of LPS from P.g in inducing autophagy in HGFs. Through a combination of morphology and quantification approaches involving autophagosomes formation observation as well as microtubule-associated protein light chain 3 (LC3)-II conversion. We further evaluated whether the PI3K/Akt/mTOR signaling could mediate LPS-induced autophagy in HGFs.

Key findings:

Our results revealed that autophagy was more obvious in LPS-treated cells compared with that in control groups. Finally, our results demonstrated that LPS from P.g promoted autophagy in HGFs and was negatively regulated by PI3K/Akt/mTOR.

Significance:

Analysis of these data implicates that LPS from P.g has a significant impact on the autophagy of HGFs by suppressing PI3K/Akt/mTOR signaling pathway.

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