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. 2018 May 16;9:1026. doi: 10.3389/fimmu.2018.01026

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Copyright © 2018 Olivares-Morales, De La Fuente, Dubois-Camacho, Parada, Diaz-Jiménez, Torres-Riquelme, Xu, Chamorro-Veloso, Naves, Gonzalez, Quera, Figueroa, Cidlowski, Vidal and Hermoso.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Glucocorticoids induce inhibition of phagocytosis in Crohn’s disease (CD). Left: the proposed model of disease indicates that bacteria such as adherent-invasive Escherichia coli (AIEC) may trigger or maintain inflammation in the gut mucosa. AIEC can infect and cross the epithelial barrier, being afterward phagocytosed by residing macrophages. Increased survival of AIEC inside macrophages induces secretion of chemokines and cytokines. Immune cells are recruited, increasing the inflammatory response and epithelium damage. Right: proposed model of glucocorticoid inducing chronicity in CD. Glucocorticoid treatment may decrease phagocytosis of AIEC by macrophages, impairing bacterial clearance. Decreased inflammatory response affects cell recruitment, which may then die through glucocorticoid-induced apoptosis. A low-grade inflammatory environment protects from epithelium damage but increases AIEC’s chances of survival, which likely perpetuates the disease.