AI Article Synopsis
- Mycobacterium tuberculosis (Mtb) is a dangerous bacteria that can severely infect humans, triggering immune responses like the release of IL-1 cytokines.
- Recent research highlights the role of IL-36, a newer member of the IL-1 family, in enhancing the immune response against Mtb by regulating cholesterol metabolism and involving the Liver X Receptor (LXR).
- Findings suggest that IL-36 affects cholesterol production and movement in infected macrophages, leading to the expression of antimicrobial peptides that help control Mtb growth, revealing a crucial link between IL-36, cholesterol metabolism, and immune defense.
Article 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.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5784124 | PMC |
| http://dx.doi.org/10.1038/s41598-018-19476-x | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Want AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!