Surfactin attenuates particulate matter‐induced COX‐2‐dependent PGE2 production in human gingival fibroblasts by inhibiting TLR2 and TLR4/MyD88/NADPH oxidase/ROS/PI3K/Akt/NF‐κB signaling pathway

Objective To evaluate the anti‐inflammatory effects of surfactin and underlying mechanisms against particulate matter (PM)‐induced inflammatory responses in human gingival fibroblasts (HGFs). Background PM, a major air pollutant, may associate with certain oral diseases possibly by inducing inflamma...

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Published in:Journal of periodontal research 2021-12, Vol.56 (6), p.1185-1199
Main Authors: Vo, Thi Thuy Tien, Wee, Yinshen, Chen, Yuh‐Lien, Cheng, Hsin‐Chung, Tuan, Vo Phuoc, Lee, I‐Ta
Format: Article
Language:English
Subjects:
1-Phosphatidylinositol 3-kinase
AKT protein
Connective tissues
Dentistry
Enzyme-linked immunosorbent assay
Fibroblasts
Gene expression
Gingiva
Immunoprecipitation
Inflammation
MyD88 protein
NAD(P)H oxidase
oral diseases
Oxidative stress
Particulate matter
Pollutants
Prostaglandin E2
Signal transduction
siRNA
Surfactin
TLR2 protein
TLR4 protein
Toll-like receptors
Transcription
Transfection
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Summary:Objective To evaluate the anti‐inflammatory effects of surfactin and underlying mechanisms against particulate matter (PM)‐induced inflammatory responses in human gingival fibroblasts (HGFs). Background PM, a major air pollutant, may associate with certain oral diseases possibly by inducing inflammation and oxidative stress. Surfactin, a potent biosurfactant, possesses various biological properties including anti‐inflammatory activity. However, the underlying mechanisms are unclear. Also, there is no study investigating the effects of surfactin on PM‐induced oral inflammatory responses. As an essential constituent of human periodontal connective tissues which involves immune‐inflammatory responses, HGFs serve as useful study models. Methods HGFs were pretreated with surfactin prior to PM incubation. The PGE2 production was determined by ELISA, while the protein expression and mRNA levels of COX‐2 and upstream regulators were measured using Western blot and real‐time PCR, respectively. The transcriptional activity of COX‐2 and NF‐κB were determined using promoter assay. ROS generation and NADPH oxidase activity were identified by specific assays. Co‐immunoprecipitation assay, pharmacologic inhibitors, and siRNA transfection were applied to explore the interplay of molecules. Mice were given one dose of surfactin or different pharmacologic inhibitors, then PM was delivered into the gingiva for three consecutive days. Gingival tissues were obtained for analyzing COX‐2 expression. Results PM‐treated HGFs released significantly higher COX‐2‐dependent PGE2, which were regulated by TLR2 and TLR4/MyD88/NADPH oxidase/ROS/PI3K/Akt/NF‐κB pathway. PM‐induced COX‐2/PGE2 increase was effectively reversed by surfactin through the disruption of regulatory pathway. Similar inhibitory effects of surfactin was observed in mice. Conclusion Surfactin may elicit anti‐inflammatory effects against PM‐induced oral inflammatory responses.
ISSN:0022-3484
1600-0765
DOI:10.1111/jre.12932