Dataset Information

Comparison of saliva from healthy and patients with dental erosion

ABSTRACT: To compare the salivary proteins from healthy and dental erosion patients to determine if there is an absence of proteins forming the enamel pellicle that may reduce their protection from acid erosion

INSTRUMENT(S): LTQ Orbitrap Velos Pro

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Saliva

SUBMITTER: Steven Lynham

LAB HEAD: Prof. Guy Carpenter

PROVIDER: PXD035565 | Pride | 2023-05-10

REPOSITORIES: Pride

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			Action	DRS
	File_Name__pr303_1.raw__F032848_.mzid.gz	Mzid
	File_Name__pr303_1.raw__F032848_.mzid_File_Name__pr303_1.raw__F032848_.MGF	Mzid
	File_Name__pr303_2.raw__F032855_.mzid.gz	Mzid
	File_Name__pr303_2.raw__F032855_.mzid_File_Name__pr303_2.raw__F032855_.MGF	Mzid
	File_Name__pr303_3.raw__F032856_.mzid.gz	Mzid

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Publications

Novel bacterial proteolytic and metabolic activity associated with dental erosion-induced oral dysbiosis.

Cleaver Leanne M LM Carda-Diéguez Miguel M Moazzez Rebeca R Carpenter Guy H GH

Microbiome 20230331 1

<h4>Background</h4>Dental erosion is a disease of the oral cavity where acids cause a loss of tooth enamel and is defined as having no bacterial involvement. The tooth surface is protected from acid attack by salivary proteins that make up the acquired enamel pellicle (AEP). Bacteria have been shown to readily degrade salivary proteins, and some of which are present in the AEP. This study aimed to explore the role of bacteria in dental erosion using a multi-omics approach by comparing saliva col ...[more]

PMID: 37004076

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Project description:Reticuloendothelial macrophages engulf ~0.2 trillion senescent erythrocytes daily in a process called erythrophagocytosis (EP). This critical mechanism preserves systemic heme-iron homeostasis by regulating red blood cell (RBC) catabolism and iron recycling. Although extensive work has demonstrated the various effects on macrophage metabolic reprogramming by stimulation with proinflammatory cytokines, little is known about the impact of EP on the macrophage metabolome and proteome. Thus, we performed mass spectrometry-based metabolomics and proteomics analyses of bone marrow-derived macrophages (BMDMs) before and after EP of IgG-coated RBCs. Further, metabolomics was performed on BMDMs incubated with free IgG to ensure that changes to macrophage metabolism were due to opsonized RBCs and not to free IgG binding. Uniformly labeled tracing experiments were conducted on BMDMs in the presence and absence of IgG-coated RBCs to assess the flux of glucose through the pentose phosphate pathway (PPP). In this study, we demonstrate that EP significantly alters amino acid and fatty acid metabolism, the Krebs cycle, OXPHOS, and arachidonate-linoleate metabolism. Increases in levels of amino acids, lipids and oxylipins, heme products, and RBC-derived proteins are noted in BMDMs following EP. Tracing experiments with U-13C6 glucose indicated a slower flux through glycolysis and enhanced PPP activation. Notably, we show that it is fueled by glucose derived from the macrophages themselves or from the extracellular media prior to EP, but not from opsonized RBCs. The PPP-derived NADPH can then fuel the oxidative burst, leading to the generation of reactive oxygen species necessary to promote digestion of phagocytosed RBC proteins via radical attack. Results were confirmed by redox proteomics experiments, demonstrating the oxidation of Cys152 and Cys94 of glyceraldehyde 3-phosphate dehydrogenase (GAPDH) and hemoglobin-β, respectively. Significant increases in early Krebs cycle and C5-branched dibasic acid metabolites (α-ketoglutarate and 2-hydroxyglutarate, respectively) indicate that EP promotes the dysregulation of mitochondrial metabolism. Lastly, EP stimulated aminolevulinic acid (ALA) synthase and arginase activity as indicated by significant accumulations of ALA and ornithine after IgG-mediated RBC ingestion. Importantly, EP-mediated metabolic reprogramming of BMDMs does not occur following exposure to IgG alone. In conclusion, we show that EP reprograms macrophage metabolism and modifies macrophage polarization.