pr8b00973_si_002.xls (59 kB)
Exploring the Arctic Charr Intestinal Glycome: Evidence of Increased N‑Glycolylneuraminic Acid Levels and Changed Host–Pathogen Interactions in Response to Inflammation
dataset
posted on 2019-03-08, 00:00 authored by Vignesh Venkatakrishnan, János T. Padra, Henrik Sundh, Kristina Sundell, Chunsheng Jin, Markus Langeland, Hanna Carlberg, Aleksander Vidakovic, Torbjörn Lundh, Niclas G. Karlsson, Sara K. LindénDisease
outbreaks are a limiting factor for the sustainable development
of the aquaculture industry. The intestinal tract is covered by a
mucus layer mainly comprised by highly glycosylated proteins called
mucins. Mucins regulate pathogen adhesion, growth, and virulence,
and the glycans are vital for these functions. We analyzed intestinal
mucin O-glycans on mucins from control and full-fat
extruded soy-bean-fed (known to cause enteritis) Arctic charr using
liquid chromatography–tandem mass spectrometry. In total, 56
glycans were identified on Arctic charr intestinal mucins, with a
high prevalence of core-5-type and sialylated O-glycans.
Disialic-acid-epitope-containing structures including NeuAcα2,8NeuAc,
NeuAc(Gc)α2,8NeuGc(Ac), and NeuGcα2,8NeuGc were the hallmark
of Arctic charr intestinal mucin glycosylation. Arctic charr fed with
soy bean meal diet had lower (i) number of structures detected, (ii)
interindividual variation, and (iii) N-glycolylneuraminic-acid-containing
glycans compared with control Arctic charr. Furthermore, Aeromonas
salmonicida grew less in response to mucins from inflamed
Arctic charr than from the control group. The Arctic charr glycan
repertoire differed from that of Atlantic salmon. In conclusion, the
loss of N-glycolylneuraminic acid may be a biomarker
for inflammation in Arctic char, and inflammation-induced glycosylation
changes affect host–pathogen interactions.