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Loss of intestinal core 1-derived O-glycans causes spontaneous colitis in mice.

Artikel i vetenskaplig tidskrift
Författare Jianxin Fu
Bo Wei
Tao Wen
Malin E V Johansson
Xiaowei Liu
Emily Bradford
Kristina A Thomsson
Samuel McGee
Lilah Mansour
Maomeng Tong
J Michael McDaniel
Thomas J Sferra
Jerrold R Turner
Hong Chen
Gunnar C. Hansson
Jonathan Braun
Lijun Xia
Publicerad i The Journal of clinical investigation
Volym 121
Nummer/häfte 4
Sidor 1657-66
ISSN 1558-8238
Publiceringsår 2011
Publicerad vid Institutionen för biomedicin, avdelningen för medicinsk kemi och cellbiologi
Sidor 1657-66
Språk en
Länkar dx.doi.org/10.1172/JCI45538
Ämneskategorier Kemi, Kemi

Sammanfattning

Mucin-type O-linked oligosaccharides (O-glycans) are primary components of the intestinal mucins that form the mucus gel layer overlying the gut epithelium. Impaired expression of intestinal O-glycans has been observed in patients with ulcerative colitis (UC), but its role in the etiology of this disease is unknown. Here, we report that mice with intestinal epithelial cell-specific deficiency of core 1-derived O-glycans, the predominant form of O-glycans, developed spontaneous colitis that resembled human UC, including massive myeloid infiltrates and crypt abscesses. The colitis manifested in these mice was also characterized by TNF-producing myeloid infiltrates in colon mucosa in the absence of lymphocytes, supporting an essential role for myeloid cells in colitis initiation. Furthermore, induced deletion of intestinal core 1-derived O-glycans caused spontaneous colitis in adult mice. These data indicate a causal role for the loss of core 1-derived O-glycans in colitis. Finally, we detected a biosynthetic intermediate typically exposed in the absence of core 1 O-glycan, Tn antigen, in the colon epithelium of a subset of UC patients. Somatic mutations in the X-linked gene that encodes core 1 β1,3-galactosyltransferase-specific chaperone 1 (C1GALT1C1, also known as Cosmc), which is essential for core 1 O-glycosylation, were found in Tn-positive epithelia. These data suggest what we believe to be a new molecular mechanism for the pathogenesis of UC.

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Utskriftsdatum: 2020-02-25