| First Author | Dong Z | Year | 2020 |
| Journal | Immunology | Volume | 160 |
| Issue | 2 | Pages | 183-197 |
| PubMed ID | 32061096 | Mgi Jnum | J:297764 |
| Mgi Id | MGI:6479241 | Doi | 10.1111/imm.13183 |
| Citation | Dong Z, et al. (2020) Histone hyperacetylation mediates enhanced IL-1beta production in LPS/IFN-gamma-stimulated macrophages. Immunology 160(2):183-197 |
| abstractText | Under the condition of lipopolysaccharide (LPS)/interferon (IFN)-gamma activation, macrophage metabolism is converted from oxidative phosphorylation to glycolysis. In the present work, we analysed whether glycolysis could affect interleukin (IL)-1beta expression through altering histone acetylation levels in mouse bone marrow-derived macrophages. Immunocytochemistry and Western blot analysis are used to characterize histone acetylation in macrophages stimulated by LPS/IFN-gamma. Real-time polymerase chain reaction and enzyme-linked immunosorbent assay were used to determine IL-1beta production. The metabolism of macrophages was monitored in real-time by the Seahorse test. Our results showed that glycolytic metabolism could enhance histone acetylation and promote IL-1beta production in LPS/IFN-gamma-activated macrophages. Moreover, increased production of IL-1beta by glycolysis was mediated through enhanced H3K9 acetylation. Importantly, it was found that a high dose of histone deacetylase inhibitor could also significantly increase the expression of IL-1beta in the absence of glycolytic metabolism. In conclusion, this study demonstrates that glycolytic metabolism could regulate IL-1beta expression by increasing histone acetylation levels in LPS/IFN-gamma-stimulated macrophages. |
