Jia Liu1, Xiaoxuan Wang1, Ming Zheng2, Qingxian Luan3. 1. Department of Periodontology, Peking University School and Hospital of Stomatology, No. 22 South Zhongguancun, Avenue, Haidian District, Beijing 100081, PR China. 2. Department of Physiology and Pathophysiology, Peking University Health Science Center, No. 38 Xueyuan Road, Haidian District, Beijing 100191, PR China. Electronic address: zhengm@bjmu.edu.cn. 3. Department of Periodontology, Peking University School and Hospital of Stomatology, No. 22 South Zhongguancun, Avenue, Haidian District, Beijing 100081, PR China. Electronic address: kqluanqx@126.com.
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.
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.
Authors: Mohamed M Meghil; Omnia K Tawfik; Mahmoud Elashiry; Mythilypriya Rajendran; Roger M Arce; David J Fulton; Patricia V Schoenlein; Christopher W Cutler Journal: Front Immunol Date: 2019-09-24 Impact factor: 7.561