Journal
JOURNAL OF IMMUNOLOGY
Volume 199, Issue 10, Pages 3466-3477Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1602016
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Funding
- National Science Foundation of China [81173633, 81503106, 81702823]
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Ungoverned activation of innate and adaptive immunity results in acute inflammatory disease, such as bacteria-induced endotoxemia and fulminant hepatitis by virus infection. Thus, therapeutic control of inflammation is crucial for clinical management of many human diseases. In murine models of LPS- and Con A-induced liver injury, we found that naringenin, a natural predominant flavanone, is capable of protecting against lethality induced by LPS and preventing inflammation-induced organ injury. The protective effect of naringenin is mediated by reducing the levels of several inflammatory cytokines. Unexpectedly, naringenin inhibits TNF-alpha and IL-6 secretion in macrophages and T cells without interfering with the TLRsignaling cascade, cytokine mRNAstability, or protein translation. These results indicate the existence of a posttranslational control mechanism. Further studies show that naringenin enhances intracellular cytokine degradation through lysosome- and TFEB-dependent mechanisms. This study provides evidence that naringenin has the capacity to dampen cytokine production by regulating lysosome function. Thus, naringenin may represent a potential therapeutic agent for controlling inflammation-related diseases.
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