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The ubiquitin system： a critical regulator of innate immunity and pathogen-host interactions

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Cellular & Molecular Immunology 2016年第5期13卷 560-576页

作者： Jie Li Qi-Yao Chai cui hua liu CAS Key Laboratory of Pathogenic Microbiology and Immunology Institute of Microbiology Chinese Academy of Sciences Beijing 100101 China

The ubiquitin system comprises enzymes that are responsible for ubiquitination and deubiquitination, as well as ubiquitin receptors that are capable of recognizing and deciphering the ubiquitin code, which act in coordination to regulate almost all host cellular processes, including host-pathogen interactions. In response to pathogen infection, the host innate immune system launches an array of distinct antimicrobial activities encompassing inflammatory signaling, phagosomal maturation, autophagy and apoptosis, all of which are fine-tuned by the ubiquitin system to eradicate the invading pathogens and to reduce concomitant host damage. By contrast, pathogens have evolved a cohort of exquisite strategies to evade host innate immunity by usurping the ubiquitin system for their own benefits. Here, we present recent advances regarding the ubiquitin system-mediated modulation of host-pathogen interplay, with a specific focus on host innate immune defenses and bacterial pathogen immune evasion.

关键词： apoptosis autophagy bacterial pathogen innate immune signaling phagosomal maturation ubiquitin system

Mycobacterium tuberculosis effector proteins: functional multiplicity and regulatory diversity

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Cellular & Molecular Immunology 2021年第5期18卷 1343-1344页

作者： Lihua Qiang Yong Zhang cui hua liu Chinese Academy of Sciences Key Laboratory of Pathogenic Microbiology and Immunology Institute of MicrobiologyChinese Academy of SciencesBeijingChina Savaid Medical School University of Chinese Academy of SciencesBeijingChina

Tuberculosis(TB),which is caused by Mycobacterium tuberculosis(Mtb),remains the leading cause of death from a single infectious ***,TB is responsible for approximately one-quarter of all deaths related to antimicrobial resistance upon the emergence of drug-resistant TB.1 Mtb infection is also associated with multiple other human diseases,such as lung cancer,autoimmune diseases,and metabolic *** Mtb lacks classical bacterial toxins(including endotoxins and exotoxins),its pathogenesis mainly involves intricate pathogen-host interplay,which is mediated by a variety of pathogenic factors,including surface-associated and secreted effector ***,a better understanding of the molecular details of the Mtb–host interaction is invaluable for the development of new therapeutic strategies against TB.

关键词： tuberculosis death Mycobacterium

Klebsiella pneumoniae NdpA suppresses ERK pathway-mediated host early inflammatory responses and is degraded through the ubiquitin-proteasome pathway

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Protein & Cell 2017年第2期8卷 144-148页

作者： Guanghua Xu Jing Wang cui hua liu CAS Key Laboratory of Pathogenic Microbiology and Immunology Institute of Microbiology Chinese Academy of Sciences Beijing 100101 China School of Life Sciences Anhui University Hefei 230601 China Savaid Medical School University of Chinese Academy of Sciences Beijing 101408 China

Klebsiella pneumoniae （KP） pathogen causing commun infections. When the host is an important opportunistic ty-acquired and nosocomial is immunocompromised, the pathogen would infect the host and cause diseases, such as pneumoniae, sepsis, liver abscess, meningitis, urinary tract inflammation and wound infection （Karaiskos et al., 2016; Park et al., 2015）. The phenomenon that K. pneumoniae has a preference to infect immunocompromised populations, especially seniors suggests that the outcomes of K. pneumoniae infection depend on the pathogen-host interactions, but up to now, the molecular mechanisms underlying K. pneumoniae-host interactions remain largely unknown.

关键词： NdpA pneumoniae Klebsiella

nsights into battles between Mycobacterium tuberculosis and macrophages

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Protein & Cell 2014年第10期5卷 728-736页

作者： Guanghua Xu Jing Wang George Fu Gao cui hua liu CAS key Laboratory of Pathogenic Microbiology and Immunology Institute of Microbiology Chinese Academy of Sciences Beijing 100101. China School of Life Sciences Anhui University Hefei 230039 China

As the first line of immune defense for Mycobacterium tuberculosis （Mtb）, macrophages also provide a major habitat for Mtb to reside in the host for years. The battles between Mtb and macrophages have been constant since ancient times. Triggered upon Mtb infection, multiple cellular pathways in macrophages are activated to initiate a tailored immune response toward the invading pathogen and regulate the cellular fates of the host as well. Toll-like receptors （TLRs） expressed on macrophages can recognize pathopatterns （PAMPs） on Mtb and mediate the production of immune-regulatory cytokines such as tumor necrosis factor （TNF） and type I Interferons （IFNs）. In addition, Vitamin D receptor （VDR） and Vitamin D-1- hydroxylase are up-regulated in Mtb-infected macrophages, by which Vitamin D participates in innate immune respon- ses. The signaling pathways that involve TNF, type I IFNs and Vitamin D are inter-connected, which play critical roles in the regulation of necroptosis, apoptosis, and autophagy of the infected macrophages. This review article summarizes cur- rent knowledge about the interactions between Mtb and macrophages, focusing on cellular fates of the Mtb-infected macrophages and the regulatory molecules and cellular pathways involved in those processes.

关键词： Mycobacterium tuberculosis,macrophages necroptosis apoptosis autophagy tumornecrosis factor (TNF) type I Interl:erons (IFNs)

Regulatory functions and mechanisms of human microbiota in infectious diseases

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hLife 2024年第10期2卷 496-513页

作者： Yingxu Fang Zehui Lei Lingqiang Zhang cui hua liu Qiyao Chai CAS Key Laboratory of Pathogen Microbiology and Immunology Institute of MicrobiologyChinese Academy of SciencesBeijingChina Savaid Medical School University of Chinese Academy of SciencesBeijingChina State Key Laboratory of Medical Proteomics Beijing Proteome Research CenterNational Center for Protein Sciences(Beijing)Beijing Institute of LifeomicsBeijingChina

The human microbiota,a diverse community of microorganisms living on or within their hosts,play an irreplaceable role in maintaining human *** of the microbiota is associated with the pathogenesis of diverse human *** recent years,growing evidence has been presented to support the substantial effect of human microbiota on the progression of infectious *** this review,we describe the functional role of human microbiota in infec-tious diseases by highlighting their Janus-faced effects in the regulation of acute and chronic infections as well as their related ***,we review the latest advances elucidating the mechanisms underlying tri-directional interactions between the microbiota,hosts,and invading pathogens,with a further discussion on external environ-mental factors that shape this interconnected regulatory network.A better understanding of the regulatory functions and mechanisms of human microbiota in infectious diseases will facilitate the development of new diagnostic,preven-tive,and therapeutic approaches for infectious diseases.

关键词： human microbiota infectious diseases co-morbidities microbiota-host-pathogen interactions environ-mental factors

Redundant Multithreading Architecture Overview

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Wuhan University Journal of Natural Sciences 2006年第6期11卷 1793-1796页

作者： YANG hua cui Gang liu Hongwei YANG Xiaozong School of Computer Science and Technology Harbin Institute of Technology Harbin 150001 Heilongjiang China

To overcome the ever-increasing susceptibility to transient-fault in processors, various redundant multithreading （RMT） architectures have been proposed, which is becoming a most effective approach for detecting and recovering from transient-fault. This paper surveys a wide range of RMT architectures-from the original AR-SMT（A-stream R-stream Simultaneous MultiThreading） to the most-recent SD-SRT （Slack-Decode Simultaneous Redundant Threading）, presenting traverse analyses and comparisons among them, and hereby demonstrates its evolution and tendency. Finally, some directions and suggestions are put forward for the further RMT research and development.

关键词： redundant multithreading processor reliability

Mycobacterium tuberculosis Mce2E suppresses the macrophage innate immune response and promotes epithelial cell proliferation

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Cellular & Molecular Immunology 2019年第4期16卷 380-391页

作者： Lihua Qiang Jing Wang Yong Zhang Pupu Ge Qiyao Chai Bingxi Li Yi Shi Lingqiang Zhang George Fu Gao cui hua liu CAS Key Laboratory of Pathogenic Microbiology and Immunology Institute of Microbiology Chinese Academy of Sciences100101 BeijingChina Institute of Health Sciences Anhui University230601 Hefei China Savaid Medical School University of Chinese Academy of Sciences 101408 Beijing China State Key Laboratory of Proteomics Beijing Proteome Research CenterNational Center of Protein Sciences BeijingBeijing Institute of Lifeomics100850 Beijing China

The intracellular pathogen Mycobacterium tuberculosis(Mtb)can survive in the host and cause disease by interfering with a variety of cellular *** mammalian cell entry 2(mce2)operon of Mtb has been shown to contribute to tuberculosis ***,little is known about the regulatory roles of Mtb Mce2 family proteins towards host cellular *** we show that the Mce2 family protein Mce2E suppressed the macrophage innate immune response and promoted epithelial cell ***2E inhibited activation of the extracellular signal-regulated kinase(ERK)and Jun N-terminal kinase(JNK)mitogen-activated protein kinase(MAPK)signaling pathways in a non-canonical D motif(a MAPK-docking motif)-dependent manner,leading to reduced expression of TNF and IL-6 in ***,Mce2E promoted proliferation of human lung epithelium-derived lung adenoma A549 cells by inhibiting K48-linked polyubiquitination of eEF1A1 in aβstrand region-dependent *** summary,Mce2E is a novel multifunctional Mtb virulence factor that regulates host cellular functions in a niche-dependent *** data suggest a potential novel target for TB therapy.

关键词： Mycobacterium tuberculosis Mce2E innate immune response cell proliferation

OTUB1 promotes osteoblastic bone formation through stabilizing FGFR2

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Signal Transduction and Targeted Therapy 2023年第5期8卷 2291-2303页

作者： Qiong Zhu Yesheng Fu Chun-Ping cui Yi Ding Zhikang Deng Chao Ning Fan Hu Chen Qiu Biyue Yu Xuemei Zhou Guan Yang Jiang Peng Weiguo Zou cui hua liu Lingqiang Zhang State Key Laboratory of Proteomics National Center for Protein Sciences(Beijing)Beijing Institute of LifeomicsBeijing100850China Lab of Orthopedics of Department of Orthopedics Beijing Key Lab of Regenerative Medicine in OrthopedicsChinese PLA General HospitalBeijing100853China Department of Endocrinology The Second Medical Center&National Clinical Research Center for Geriatric DiseasesChinese PLA General HospitalBeijing100853China School of Life Sciences Hebei UniversityBaodingHebei071002China State Key Laboratory of Cell Biology Shanghai Institute of Biochemistry and Cell BiologyCenter for Excellence in Molecular Cell ScienceChinese Academy of SciencesUniversity of Chinese Academy of SciencesShanghai200031China CAS Key Laboratory of Pathogenic Microbiology and Immunology Institute of MicrobiologyChinese Academy of SciencesBeijing100101China Savaid Medical School University of Chinese Academy of SciencesBeijing101408China

Bone homeostasis is maintained by the balance between osteoblastic bone formation and osteoclastic bone *** of this process leads to multiple diseases,including ***,the underlying molecular mechanisms are not fully ***,we show that the global and conditional osteoblast knockout of a deubiquitinase Otub1 result in low bone mass and poor bone strength due to defects in osteogenic differentiation and ***,the stability of FGFR2,a crucial regulator of osteogenesis,is maintained by ***1 attenuates the E3 ligase SMURF1-mediated FGFR2 ubiquitination by inhibiting SMURF1’s E2 *** the absence of OTUB1,FGFR2 is ubiquitinated excessively by SMURF1,followed by lysosomal ***,adeno-associated virus serotype 9(AAV9)-delivered FGFR2 in knee joints rescued the bone mass loss in osteoblast-specific Otub1-deleted ***,Otub1 mRNA level was significantly downregulated in bones from osteoporotic mice,and restoring OTUB1 levels through an AAV9-delivered system in ovariectomy-induced osteoporotic mice attenuated *** together,our results suggest that OTUB1 positively regulates osteogenic differentiation and mineralization in bone homeostasis by controlling FGFR2 stability,which provides an optical therapeutic strategy to alleviate osteoporosis.

关键词： FGFR2 homeostasis maintained

The deubiquitinase OTUD1 inhibits colonic inflammation by suppressing RIPK1-mediated NF-κB signaling

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Cellular & Molecular Immunology 2022年第2期19卷 276-289页

作者： Bo Wu Lihua Qiang Yong Zhang Yesheng Fu Mengyuan Zhao Zehui Lei Zhe Lu Yan-Ge Wei Hongmiao Dai Yingwei Ge Mingqiu liu Xuemei Zhou Zhiqiang Peng Hongchang Li Chun-Ping cui Jing Wang Hui Zheng cui hua liu Lingqiang Zhang State Key Laboratory of Proteomics National Center for Protein Sciences(Beijing)Beijing Institute of LifeomicsBeijing100850China CAS Key Laboratory of Pathogenic Microbiology and Immunology Institute of MicrobiologyChinese Academy of SciencesBeijing100101China Savaid Medical School University of Chinese Academy of SciencesBeijing101408China International Institute of Infection and Immunity Institutes of Biology and Medical SciencesSoochow UniversitySuzhouJiangsuChina

The E3 ubiquitin ligase(E3)-mediated ubiquitination and deubiquitinase(DUB)-mediated deubiquitination processes are closely associated with the occurrence and development of colonic *** tumor deubiquitinase 1(OTUD1)is involved in immunoregulatory functions linked to infectious ***,the effect of OTUD1 on intestinal immune responses during colonic inflammatory disorders such as inflammatory bowel disease(IBD)remains ***,we show that loss of OTUD1 in mice contributes to the pathogenesis of dextran sulfate sodium(DSS)-induced colitis via excessive release of proinflammatory *** addition,bone marrow transplantation experiments revealed that OTUD1 in hematopoietic cells plays a dominant role in protection against ***,OTUD1 physically interacts with receptor-interacting serine/threonine-protein kinase 1(RIPK1)and selectively cleaves K63-linked polyubiquitin chains from RIPK1 to inhibit the recruitment of NF-κB essential modulator(NEMO).Moreover,the expression of OTUD1 in mucosa samples from ulcerative colitis(UC)patients was lower than that in mucosa samples from healthy ***,we demonstrate that the UC-associated OTUD1 G430V mutation abolishes the ability of OTUD1 to inhibit RIPK1-mediated NF-κB activation and intestinal *** together,our study unveils a previously unexplored role of OTUD1 in moderating intestinal inflammation by inhibiting RIPK1-mediated NF-κB activation,suggesting that the OTUD1-RIPK1 axis could be a potential target for the treatment of IBD.

关键词： OTUD1 RIPK1 NF-κB IBD