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Plasma N-glycome composition associates with chronic low back pain

Research output: Contribution to journalArticle

Irena Trbojević-Akmačić, Frano Vučković, Marija Vilaj, Andrea Skelin, Lennart C. Karssen, Jasminka Krištić, Julija Jurić, Ana Momčilović, Jelena Šimunović, Massimo Mangino, Manuela De Gregori, Maurizio Marchesini, Concetta Dagostino, Jerko Štambuk, Mislav Novokmet, Richard Rauck, Yurii S. Aulchenko, Dragan Primorac, Leonardo Kapural, Klaas Buyse & 5 more Dieter Mesotten, Frances M.K. Williams, Jan van Zundert, Massimo Allegri, Gordan Lauc

Original languageEnglish
JournalBIOCHIMICA ET BIOPHYSICA ACTA-GENERAL SUBJECTS
Early online date5 Jul 2018
DOIs
Publication statusE-pub ahead of print - 5 Jul 2018

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Abstract

Background Low back pain (LBP) is the symptom of a group of syndromes with heterogeneous underlying mechanisms and molecular pathologies, making treatment selection and patient prognosis very challenging. Moreover, symptoms and prognosis of LBP are influenced by age, gender, occupation, habits, and psychological factors. LBP may be characterized by an underlying inflammatory process. Previous studies indicated a connection between inflammatory response and total plasma N-glycosylation. We wanted to identify potential changes in total plasma N-glycosylation pattern connected with chronic low back pain (CLBP), which could give an insight into the pathogenic mechanisms of the disease. Methods Plasma samples of 1128 CLBP patients and 760 healthy controls were collected in clinical centers in Italy, Belgium and Croatia and used for N-glycosylation profiling by hydrophilic interaction ultra-performance liquid chromatography (HILIC-UPLC) after N-glycans release, fluorescent labeling and clean-up. Observed N-glycosylation profiles have been compared with a cohort of 126 patients with acute inflammation that underwent abdominal surgery. Results We have found a statistically significant increase in the relative amount of high-branched (tri-antennary and tetra-antennary) N-glycan structures on CLBP patients' plasma glycoproteins compared to healthy controls. Furthermore, relative amounts of disialylated and trisialylated glycan structures were increased, while high-mannose and glycans containing bisecting N-acetylglucosamine decreased in CLBP. Conclusions Observed changes in CLBP on the plasma N-glycome level are consistent with N-glycosylation changes usually seen in chronic inflammation. General significance To our knowledge, this is a first large clinical study on CLBP patients and plasma N-glycome providing a new glycomics perspective on potential disease pathology.

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