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IL-36/LXR axis modulates cholesterol metabolism and immune defense to Mycobacterium tuberculosis

Abstract:
Mycobacterium tuberculosis (Mtb) is a life-threatening pathogen in humans. Bacterial infection of macrophages usually triggers strong innate immune mechanisms, including IL-1 cytokine secretion. The newer member of the IL-1 family, IL-36, was recently shown to be involved in cellular defense against Mtb. To unveil the underlying mechanism of IL-36 induced antibacterial activity, we analyzed its role in the regulation of cholesterol metabolism, together with the involvement of Liver X Receptor (LXR) in this process. We report that, in Mtb-infected macrophages, IL-36 signaling modulates cholesterol biosynthesis and efflux via LXR. Moreover, IL-36 induces the expression of cholesterol-converting enzymes and the accumulation of LXR ligands, such as oxysterols. Ultimately, both IL-36 and LXR signaling play a role in the regulation of antimicrobial peptides expression and in Mtb growth restriction. These data provide novel evidence for the importance of IL-36 and cholesterol metabolism mediated by LXR in cellular host defense against Mtb.
Publication status:
Published
Peer review status:
Peer reviewed

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Publisher copy:
10.1038/s41598-018-19476-x

Authors


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Role:
Author
ORCID:
0000-0001-9866-8268
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Institution:
University of Oxford
Division:
Medical Sciences Division
Department:
NDM
Department:
Oxford. MSD, NDM
Role:
Author
ORCID:
0000-0003-4337-9113


Publisher:
Springer Nature
Journal:
Scientific Reports More from this journal
Volume:
8
Article number:
1520
Publication date:
2018-01-24
Acceptance date:
2017-12-27
DOI:
EISSN:
2045-2322
Pmid:
29367626


Language:
English
Pubs id:
pubs:939832
UUID:
uuid:69c88c8c-c42d-49fb-9b31-f2a2073ac8d7
Local pid:
pubs:939832
Source identifiers:
939832
Deposit date:
2018-11-09

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