NDLI: NLRP3 Triggers Attenuate Lipocalin-2 Expression Independent with Inflammasome Activation

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NLRP3 Triggers Attenuate Lipocalin-2 Expression Independent with Inflammasome Activation

Content Provider	MDPI
Author	Ahn, Huijeong Lee, Gilyoung Kim, Jeongeun Park, Jeongho Kang, Seung Yoon, Sung-Il Lee, Eunsong Lee, Geun-Shik
Copyright Year	2021
Description	Lipocalin-2 (LCN2), a small secretory glycoprotein, is upregulated by toll-like receptor (TLR) signaling in various cells and tissues. LCN2 inhibits bacterial growth by iron sequestration and regulates the innate immune system. Inflammasome activates the inflammatory caspases leading to pyroptosis and cytokine maturation. This study examined the effects of inflammasome activation on LCN2 secretion in response to TLR signaling. The triggers of NLRP3 inflammasome activation attenuated LCN2 secretion while it induced interleukin-1β in mouse macrophages. In mice, NLRP3 inflammasome activation inhibited TLR-mediated LCN2 secretion. The inhibition of NLRP3 triggers on LCN2 secretion was caused by the inhibited transcription and translation of LCN2. At the same time, no changes in the other cytokines and IκBζ, a well-known transcriptional factor of Lcn2 transcription, were observed. Overall, NLRP3 triggers are a regulator of LCN2 expression suggesting a new linkage of inflammasome activation and LCN2 secretion in the innate immunity.
Starting Page	1660
e-ISSN	20734409
DOI	10.3390/cells10071660
Journal	Cells
Issue Number	7
Volume Number	10
Language	English
Publisher	MDPI
Publisher Date	2021-07-02
Access Restriction	Open
Subject Keyword	Cells Immunology Lipocalin-2 Nlrp3 Inflammasome Nigericin Macrophages
Content Type	Text
Resource Type	Article

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