Please use this identifier to cite or link to this item: http://hdl.handle.net/2445/171050
Title: The influenza virus NS1A binding protein gene modulates macrophages response to cytokines and phagocytic potential in inflammation
Author: Hotter, Georgina
Mastora, Chrysoula
Jung, Michaela
Brüne, Bernhard, 1957-
Carbonell i Camós, Teresa
Josa, Claudia
Pérez-Calvo, Juan Ignacio
Cruzado, Josep Ma.
Guiteras, Roser
Sola, Anna
Keywords: Virologia
Virology
Issue Date: 17-Sep-2020
Publisher: Nature Publishing Group
Abstract: Macrophages show remarkable phenotypic plasticity in response to environmental signals. Although it is generally less considered, cytoskeletal changes in macrophages influence their phenotype, including phagocytosis and secretion of soluble cytokines. Influenza virus NS1A-binding protein (Ivns1abp) belongs to the Kelch family of proteins that play a central role in actin cytoskeleton dynamics by directly associating with F-actin and by protecting against actin derangement. Due to its role in cytoskeleton preservation, the Ivns1abp gene might be a critical regulator of the macrophage phenotype and function under inflammatory conditions. In this study, we determine that the modulation of the Ivns1abp gene in macrophages could modify resistance to macrophages against inflammation and maintain functional phagocytosis. Our results indicate that inflammatory insults inhibit the Ivns1abp gene, whereby phagocytosis is inhibited and the ability of macrophages to induce proliferation and repair of damaged cells is compromised. Furthermore, our results show that inflammatory insults alter the activity of the transcription factor c-myc, a factor which directly modulates the expression of the Ivns1abp gene. In conclusion, this study demonstrates a central role of lvns1abp in promoting and preserving a reparative macrophage phenotype and resistance to this inflammatory environment.
Note: Reproducció del document publicat a: https://doi.org/10.1038/s41598-020-72342-7
It is part of: Scientific Reports, 2020, vol. 10, p. 15302
URI: http://hdl.handle.net/2445/171050
Related resource: https://doi.org/10.1038/s41598-020-72342-7
ISSN: 2045-2322
Appears in Collections:Articles publicats en revistes (Biologia Cel·lular, Fisiologia i Immunologia)

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