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. 2019 Nov 20;10:2449. doi: 10.3389/fimmu.2019.02449

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Copyright © 2019 Dubois-Camacho, Diaz-Jimenez, De la Fuente, Quera, Simian, Martínez, Landskron, Olivares-Morales, Cidlowski, Xu, Gao, Xie, Chnaiderman, Soto-Rifo, González, Calixto 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(s) 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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TNFα decreases miR-378a-3p and increases IL-33 expression in colonocytes. HT-29 cell line was stimulated with 10 ng/mL human recombinant TNFα (hr-TNFα) for 3, 6, and 24 h. Fold change relative to non-stimulated control of (A) MiR-378a-3p and (B) IL-33 mRNA. (C) IL-33 protein was measured in HT-29 cells stimulated with hr-TNFα 10 ng/mL 12, 24, and 48 h by WB, (D) Band quantification of IL-33 protein normalized to β-actin. (E) Fold change relative to non-stimulated control of PPARGC1B mRNA and (F) IL-8 mRNA levels (measured as control of TNFα stimulus). (G) AGO1 and (H) AGO2 mRNA levels were assessed as control of miRNA-biogenesis machinery. Four experiments by duplicated were analyzed using Two-way ANOVA with Bonferroni post-test. *P < 0.05, **P = < 0.01.