Bitter receptor TAS2R138 facilitates lipid droplet degradation in neutrophils during Pseudomonas aeruginosa infection  

作　　者：Qinqin Pu Kai Guo Ping Lin Zhihan Wang Shugang Qin Pan Gao Colin Combs Nadeem Khan Zhenwei Xia Min Wu 

机构地区：[1]Department of Biomedical Sciences,School of Medicine and Health Sciences,University of North Dakota,Grand Forks,ND,USA [2]Department of Neurology,University of Michigan,Ann Arbor,Ml,USA [3]Wound Trauma Medical Center,State Key Laboratory of Trauma,Burns and Combined Injury,Daping Hospital,Army Medical University,Chongqing,China [4]Biological Science Research Center,Southwest University,Chongqing 400716,China [5]West China School of Basic Medical Sciences&Forensic Medicine,Sichuan University,Chengdu,Sichuan,China [6]State Key Laboratory of Biotherapy and Cancer Center,West China Hospital,Sichuan University,and Collaborative Innovation Center for Biotherapy,Chengdu,Sichuan,China [7]Department of Pediatrics,Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine,Shanghai,People's Republic of China

出　　处：《Signal Transduction and Targeted Therapy》2021年第7期2154-2163,共10页信号转导与靶向治疗（英文）

基　　金：The authors thank the National Institutes of Health for Grants R01 AM 138203,R01 All09317-01 Al,and AI097532-01A1 for M.W.,as well as P20 GM113123 and P20 GM103442 for Imaging,Histology,and Flow Cytometry Core Facility.

摘　　要：Bitter receptors function primarily in sensing taste,but may also have other functions,such as detecting pathogenic organisms due to their agile response to foreign objects.The mouse taste receptor type-2 member 138(TAS2R138)is a member of the G-protein-coupled bitter receptor family,which is not only found in the tongue and nasal cavity,but also widely distributed in other organs,such as the respiratory tract,gut,and lungs.Despite its diverse functions,the role of TAS2R138 in host defense against bacterial infection is largely unknown.Here,we show that TAS2R138 facilitates the degradation of lipid droplets(LDs)in neutrophils during Pseudomonas aeruginosa infection through competitive binding with PPARG(peroxisome proliferator-activated receptor gamma)antagonist:A/-(3-oxododecanoyl)-L-homoserine lactone(AHL-12),which coincidently is a virulence-bound signal produced by this bacterium(P.aeruginosa).The released PPARG then migrates from nuclei to the cytoplasm to accelerate the degradation of LDs by binding PLIN2(perilipin-2).Subsequently,the TAS2R138-AHL-12 complex targets LDs to augment their degradation,and thereby facilitating the clearance of AHL-12 in neutrophils to maintain homeostasis in the local environment.These findings reveal a crucial role for TAS2R138 in neutrophil-mediated host immunity against P.aeruginosa infection.

关 键 词：thereby MAINTAIN MIGRATE 

分 类 号：R392[医药卫生—免疫学]