IL-22 promotes formation of MUC17 glycocalyx barrier in postnatal small intestine during weaning. Layunta et al.

Published: 4 February 2021| Version 1 | DOI: 10.17632/g6wp3mbwwz.1
Contributor:
Thaher Pelaseyed

Description

The intestine is under constant exposure to chemicals, antigens and microorganisms from the external environment. Apical aspects of absorptive epithelial cells form a brush border membrane (BBM), shaped by packed microvilli coated with a dense glycocalyx. We present evidence showing that the glycocalyx forms an epithelial barrier that prevents exogenous molecules and live bacteria from gaining access to BBM. We use a multi-omics approach to investigate function and regulation of membrane mucins exposed on the BBM during postnatal development of mouse small intestine. Muc17 is identified as a major membrane mucin in the glycocalyx that is specifically upregulated by IL-22 as part of an epithelial defense repertoire during weaning. High levels of IL-22 at time of weaning reprogram neonatal postmitotic progenitor enterocytes to differentiate into Muc17-expressing enterocytes, as found in adult intestine during homeostasis. Our findings propose a role for Muc17 in epithelial barrier function in small intestine.

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