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Advanced glycation end products impair NLRP3 inflammasome-mediated innate immune responses in macrophages

Authors
Son, SeunghwanHwang, InhwaHan, Seung HyeokShin, Jeon-SooShin, Ok SarahYu, Je-Wook
Issue Date
15-12월-2017
Publisher
AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
Keywords
glycation; inflammasome; innate immunity; macrophage; NLRP3
Citation
JOURNAL OF BIOLOGICAL CHEMISTRY, v.292, no.50, pp.20437 - 20448
Indexed
SCIE
SCOPUS
Journal Title
JOURNAL OF BIOLOGICAL CHEMISTRY
Volume
292
Number
50
Start Page
20437
End Page
20448
URI
https://scholar.korea.ac.kr/handle/2021.sw.korea/81162
DOI
10.1074/jbc.M117.806307
ISSN
0021-9258
Abstract
Advanced glycation end products (AGEs) are adducts formed on proteins by glycation with reducing sugars, such as glucose, and tend to form and accumulate under hyperglycemic conditions. AGE accumulation alters protein function and has been implicated in the pathogenesis of many degenerative diseases such as diabetic complications. AGEs have also been shown to promote the production of pro-inflammatory cytokines, but the roles of AGEs in inflammasome signaling have not been explored in detail. Here, we present evidence that AGEs attenuate activation of the NLRP3 inflammasome in bone marrow-derived macrophages (BMDMs) as determined by caspase-1 processing and interleukin-1 production. AGEs also dampened the assembly of the NLRP3 inflammasome, but did not affect the NLRC4 or AIM2 inflammasome activation. Moreover, our data indicated that AGE treatment inhibited Toll-like receptor (TLR)-dependent production of pro-inflammatory cytokines in BMDMs. This immunosuppressive effect of AGE was not associated with a receptor for AGEs (RAGE)-mediated signaling. Instead, AGE treatment markedly suppressed lipopolysaccharide-induced M1 polarization of macrophages. Furthermore, AGEs significantly dampened innate immune responses including NLRP3 inflammasome activation and type-I interferon production in macrophages upon influenza virus infection. These observations collectively suggest that AGEs could impair host NLRP3 inflammasome-mediated innate immune defenses against RNA virus infection leading to an increased susceptibility to infection.
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