title: Plant Lectins Activate the NLRP3 Inflammasome To Promote Inflammatory Disorders.
abstract: Plant-derived dietary lectins have been reported to be involved in the pathogenesis of several inflammatory diseases, including inflammatory bowel disease, diabetes, rheumatoid arthritis, and celiac disease, but little is known about the molecular mechanisms underlying lectin-induced inflammation. In this study, we showed that plant lectins can induce caspase-1 activation and IL-1β secretion via the NLRP3 inflammasome. Lectins were internalized and subsequently escaped from the lysosome and then translocated to the endoplasmic reticulum. Endoplasmic reticulum-loaded plant lectins then triggered Ca2+release and mitochondrial damage, and inhibition of Ca2+release and mitochondrial reactive oxygen species by chemical inhibitors significantly suppressed NLRP3 inflammasome activation. In vivo, plant lectin-induced inflammation and tissue damage also depended on the NLRP3 inflammasome. Our findings indicate that plant lectins can act as an exogenous "danger signal" that can activate the NLRP3 inflammasome and suggest that dietary lectins might promote inflammatory diseases via the NLRP3 inflammasome.
authors.affiliation: Institute of Immunology and the Chinese Academy of Sciences Key Laboratory of Innate Immunity and Chronic Disease, Chinese Academy of Sciences Center for Excellence in Molecular Cell Sciences, School of Life Sciences and Medical Center, University of Science and Technology of China, Hefei 230027, China.
authors.forename: Tao
authors.identifier: 0000-0002-9414-6902
authors.initials: T
authors.lastname: Gong
authors.affiliation: Institute of Immunology and the Chinese Academy of Sciences Key Laboratory of Innate Immunity and Chronic Disease, Chinese Academy of Sciences Center for Excellence in Molecular Cell Sciences, School of Life Sciences and Medical Center, University of Science and Technology of China, Hefei 230027, China.
authors.forename: Xiaqiong
authors.identifier: 0000-0001-9519-1732
authors.initials: X
authors.lastname: Wang
authors.affiliation: Institute of Immunology and the Chinese Academy of Sciences Key Laboratory of Innate Immunity and Chronic Disease, Chinese Academy of Sciences Center for Excellence in Molecular Cell Sciences, School of Life Sciences and Medical Center, University of Science and Technology of China, Hefei 230027, China.
authors.forename: Yanqing
authors.initials: Y
authors.lastname: Yang
authors.affiliation: Institute of Immunology and the Chinese Academy of Sciences Key Laboratory of Innate Immunity and Chronic Disease, Chinese Academy of Sciences Center for Excellence in Molecular Cell Sciences, School of Life Sciences and Medical Center, University of Science and Technology of China, Hefei 230027, China.
authors.forename: Yiqing
authors.identifier: 0000-0002-3813-849X
authors.initials: Y
authors.lastname: Yan
authors.affiliation: Department of Gastroenterology, Nanjing Drum Tower Hospital, Affiliated Hospital of Nanjing University Medical School, Nanjing University, Nanjing 210008, China.
authors.forename: Chenggong
authors.identifier: 0000-0001-8249-8321
authors.initials: C
authors.lastname: Yu
authors.affiliation: Institute of Immunology and the Chinese Academy of Sciences Key Laboratory of Innate Immunity and Chronic Disease, Chinese Academy of Sciences Center for Excellence in Molecular Cell Sciences, School of Life Sciences and Medical Center, University of Science and Technology of China, Hefei 230027, China.|Innovation Center for Cell Signaling Network, University of Science and Technology of China, Hefei 230027, China.|Hefei National Laboratory for Physical Sciences at Microscale, University of Science and Technology of China, Hefei 230027, China; and.|State Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Signaling Network, School of Life Sciences, Xiamen University, Xiamen 361101, China.
authors.forename: Rongbin
authors.initials: R
authors.lastname: Zhou
authors.affiliation: Institute of Immunology and the Chinese Academy of Sciences Key Laboratory of Innate Immunity and Chronic Disease, Chinese Academy of Sciences Center for Excellence in Molecular Cell Sciences, School of Life Sciences and Medical Center, University of Science and Technology of China, Hefei 230027, China; ustcjw@ustc.edu.cn.|Hefei National Laboratory for Physical Sciences at Microscale, University of Science and Technology of China, Hefei 230027, China; and.
authors.forename: Wei
authors.initials: W
authors.lastname: Jiang
mesh_terms: D000818:Animals; D001327:Autoimmune Diseases / Q000276:immunology*; D020013:Calcium Signaling; D032449:Canavalia / Q000276:immunology*; D020170:Caspase 1 / Q000378:metabolism; D004032:Diet; D004721:Endoplasmic Reticulum / Q000378:metabolism; D006801:Humans; D058847:Inflammasomes / Q000378:metabolism*; D007249:Inflammation / Q000276:immunology*; D053583:Interleukin-1beta / Q000378:metabolism; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D008928:Mitochondria / Q000378:metabolism*; D000071199:NLR Family, Pyrin Domain-Containing 3 Protein / Q000378:metabolism*; D037121:Plant Lectins / Q000276:immunology / Q000378:metabolism*; D017382:Reactive Oxygen Species / Q000378:metabolism
chemical_list: D058847:Inflammasomes; D053583:Interleukin-1beta; D000071199:NLR Family, Pyrin Domain-Containing 3 Protein; C492716:Nlrp3 protein, mouse; D037121:Plant Lectins; D017382:Reactive Oxygen Species; D020170:Caspase 1