Dataset Information

Lipidomic analysis reveals altered lipid profiles of clinically healthy and periodontitis-affected gingival biopsies

ABSTRACT:

AIM: The role of lipids in periodontitis has not been well studied. Thus, this study aimed to explore periodontitis-associated lipid profile changes and identify differentially expressed lipid metabolites in gingival tissues.

MATERIALS AND METHODS: Gingival tissues from 38 patients with periodontitis (periodontitis group) and 38 periodontally healthy individuals (control group) were collected. A UHPLC-QTOF-MS-based non-targeted metabolomics platform was used to identify and compare the lipid profiles of the two groups. The distribution and expression of related proteins were subsequently analyzed via immunohistochemistry to further validate the identified lipids.

RESULTS: Lipid profiles significantly differed between the two groups, and 20 differentially expressed lipid species were identified. Lysophosphatidylcholines (lysoPCs), diacylglycerols (DGs) and phosphatidylethanolamines (PEs) were significantly upregulated, while triacylglycerols (TGs) were downregulated in the periodontitis group. Moreover, the staining intensity of ABHD5/CGI-58, secretory phospholipase A2 (sPLA2), and sPLA2-IIA was significantly stronger in the gingival tissues of patients with periodontitis than in those of healthy controls.

CONCLUSIONS: LysoPCs, DGs, and PEs were significantly upregulated, whereas TGs were downregulated in gingival tissues of patients with periodontitis. Correspondingly, the immunohistochemical staining of ABHD5/CGI-58, sPLA2 and sPLA2-IIA in gingival tissues was consistent with the downstream production of lipid classes (lysoPCs, TGs and DGs).

INSTRUMENT(S): Liquid Chromatography MS - positive - reverse phase

SUBMITTER: Min Zhou

PROVIDER: MTBLS4684 | MetaboLights | 2022-08-19

REPOSITORIES: MetaboLights

ACCESS DATA

Similar Datasets

Project description:Purpose: The goals of this study are to compare the difference between WT and hCD147 mice, hACE2 and hCD147 mice lung tissues Transcriptomes after infection with SARS-CoV-2 Methods: After receiving anesthesia with pentobarbital sodium, each mouse of the WT group, hCD147 group, and hACE2 group was infected with SARS-CoV-2 by nasal drip at a dose of 3 x 10^5 TCID50. The lung tissues were take for RNA-seq at 2 dpi. each mouse of the hCD147 group, and hACE2 group was infected with SARS-CoV-2 by nasal drip at a dose of 3 x 10^5 TCID50. The lung tissues were take for RNA-seq at 2 dpi. Results: RNA-seq of lung homogenates from C57BL/6 and hCD147 mice at 2 d.p.i. showed 354 upregulated and 175 downregulated genes). hCD147 mice mediated strong inflammatory responses, including Th17 cell responses, the NF-kappaB pathway and MAPK pathway, etc. The levels of cytokines and chemokines were increased in the lung of hCD147 mice, such as IL6, IL10, ILbeta, CXCL1, CXCL2, CCL2, etc. Analysis of RNA-Seq data of hACE2 mice versus hCD147 mice showed that hACE2 mice had stronger antiviral responses, including type I IFN and IFNalpha/IFNbeta responses, while hCD147 mice showed activation of multiple proinflammatory pathways, which is consistent with clinical features of COVID-19 patients. The significantly upregulated genes during SARS-CoV-2 infection of hACE2 mice enriched in cellular response to IFN-?. The upregulated genes in SARS-CoV-2-infected hCD147 mice were enriched secretory proteins, including ILbeta, IL6 and CXCL1. Conclusions: CD147 mediates potent inflammatory responses in SARS-CoV-2 infection. RNA-seq of lung homogenates from hACE2 and hCD147 mice at 2 d.p.i. showed 354 upregulated and 175 downregulated genes). hCD147 mice mediated strong inflammatory responses, including Th17 cell responses, the NF-kappaB pathway and MAPK pathway, etc. The levels of cytokines and chemokines were increased in the lung of hCD147 mice, such as IL6, IL10, ILbeta, CXCL1, CXCL2, CCL2, etc.

Dataset Information

Lipidomic analysis reveals altered lipid profiles of clinically healthy and periodontitis-affected gingival biopsies

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure