AI Article Synopsis
- The study investigates the role of IgG -glycosylation in chronic thromboembolic pulmonary hypertension (CTEPH) to understand its inflammatory mechanisms and identify potential new markers and therapies.
- Researchers analyzed the plasma IgG -glycome in CTEPH patients, finding decreased IgG galactosylation associated with a proinflammatory state and strong connections to clinical markers like NT-proBNP.
- This groundbreaking research is the first to map the IgG -glycome's proinflammatory phenotype in CTEPH, highlighting its potential as an indicator of inflammation and enhancing our understanding of the disease's glycomic mechanisms.
Article Abstract
Background: The pathological mechanism of chronic thromboembolic pulmonary hypertension (CTEPH) is not fully understood, and inflammation has been reported to be one of its etiological factors. IgG regulates systemic inflammatory homeostasis, primarily through its -glycans. Little is known about IgG -glycosylation in CTEPH. We aimed to map the IgG -glycome of CTEPH to provide new insights into its pathogenesis and discover novel markers and therapies.
Methods: We characterized the plasma IgG -glycome of patients with CTEPH in a discovery cohort and validated our results in an independent validation cohort using matrix-assisted laser desorption/ionization time of flight mass spectrometry. Thereafter, we correlated IgG -glycans with clinical parameters and circulating inflammatory cytokines in patients with CTEPH. Furthermore, we determined IgG -glycan quantitative trait loci in CTEPH to reveal partial mechanisms underlying glycan changes.
Results: Decreased IgG galactosylation representing a proinflammatory phenotype was found in CTEPH. The distribution of IgG galactosylation showed a strong association with NT-proBNP (N-terminal pro-B-type natriuretic peptide) in CTEPH. In line with the glycomic findings, IgG pro-/anti-inflammatory -glycans correlated well with a series of inflammatory markers and gene loci that have been reported to be involved in the regulation of these glycans or inflammatory immune responses.
Conclusions: This is the first study to reveal the full signature of the IgG -glycome of a proinflammatory phenotype and the genes involved in its regulation in CTEPH. Plasma IgG galactosylation may be useful for evaluating the inflammatory state in patients with CTEPH; however, this requires further validation. This study improves our understanding of the mechanisms underlying CTEPH inflammation from the perspective of glycomics.
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| http://dx.doi.org/10.1161/HYPERTENSIONAHA.123.21408 | DOI Listing |
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