Format

Send to

Choose Destination
Sci Rep. 2017 Apr 12;7(1):838. doi: 10.1038/s41598-017-00828-y.

Global analysis of glycoproteins identifies markers of endotoxin tolerant monocytes and GPR84 as a modulator of TNFα expression.

Author information

1
Septomics Research Center, Jena University Hospital, Jena, Germany.
2
Jena University Hospital, Integrated Research and Treatment Center - Center for Sepsis Control and Care (CSCC), Jena, Germany.
3
Leibnitz Institute for Natural Product Research and Infection Biology - Hans-Knöll-Institut, Jena, Germany.
4
BioControl Jena GmbH, Jena, Germany.
5
Septomics Research Center, Jena University Hospital, Jena, Germany. Hortense.Slevogt@med.uni-jena.de.

Abstract

Exposure of human monocytes to lipopolysaccharide (LPS) induces a temporary insensitivity to subsequent LPS challenges, a cellular state called endotoxin tolerance. In this study, we investigated the LPS-induced global glycoprotein expression changes of tolerant human monocytes and THP-1 cells to identify markers and glycoprotein targets capable to modulate the immunosuppressive state. Using hydrazide chemistry and LC-MS/MS analysis, we analyzed glycoprotein expression changes during a 48 h LPS time course. The cellular snapshots at different time points identified 1491 glycoproteins expressed by monocytes and THP-1 cells. Label-free quantitative analysis revealed transient or long-lasting LPS-induced expression changes of secreted or membrane-anchored glycoproteins derived from intracellular membrane coated organelles or from the plasma membrane. Monocytes and THP-1 cells demonstrated marked differences in glycoproteins differentially expressed in the tolerant state. Among the shared differentially expressed glycoproteins G protein-coupled receptor 84 (GPR84) was identified as being capable of modulating pro-inflammatory TNFα mRNA expression in the tolerant cell state when activated with its ligand Decanoic acid.

PMID:
28404994
PMCID:
PMC5429802
DOI:
10.1038/s41598-017-00828-y
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Nature Publishing Group Icon for PubMed Central
Loading ...
Support Center