Tingting Xu

Hubei Provincial Water Resources and Hydropower Planning Survey and Design Institute

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Mengqi Qian

Zhejiang University

Zhiren Yang

Zhejiang University

Kai Zhou

Chinese Academy of Fishery Sciences

Xinchen Zhou

Zhejiang University

Xinyan Han

Ministry of Agriculture and Rural Affairs

Xiaoyun Xu

Northeast Normal University

Qingli Zhang

State Key Laboratory of Food Science and Technology

Ting Wu

Southern Medical University

Meng Li

Zhejiang University

Siyi Pan

Huazhong Agricultural University

Cooperative Institutions

Chinese Academy of Sciences

Ministry of Agriculture and Rural Affairs

Huazhong Agricultural University

Chinese Academy of Fishery Sciences

Zhejiang University

Qingdao National Laboratory for Marine Science and Technology

University of Chinese Academy of Sciences

Chinese Academy of Medical Sciences & Peking Union Medical College

Nankai University

Southern University of Science and Technology

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A fructose/H+ symporter controlled by a LacI-type regulator promotes survival of pandemic Vibrio cholerae in seawater

Nature Communications (2021)

Yutao Liu Bin Liu Tingting Xu Qian Wang Wen‐Di Li

The bacterium Vibrio cholerae can colonize the human intestine and cause cholera, but spends much of its life cycle in seawater. The pathogen must adapt to substantial environmental changes when moving between seawater and the human intestine, including different availability of carbon sources such as fructose. Here, we use in vitro experiments as well as mouse intestinal colonization assays to study the mechanisms used by pandemic V. cholerae to adapt to these environmental changes. We show that a LacI-type regulator (FruI) and a fructose/H

10.1038/s41467-021-24971-3

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Citations (8)

MOESM2 of RstA, a two-component response regulator, plays important roles in multiple virulence-associated processes in enterohemorrhagic Escherichia coli O157:H7

Figshare (2019)

Yutao Liu Shujie Li Wen‐Di Li Peisheng Wang Peng Ding

Additional file 2: Excel file S1. Down-regulated genes in the ΔrstA mutant compared with EHEC O157:H7 wild type strain, Excel file S2. Up-regulated genes in the ΔrstA mutant compared with EHEC O157:H7 wild type strain. Excel file S3. Differently expressed LEE genes in the ΔrstA mutant compared with EHEC O157:H7 wild type strain, Excel file S4. Differently expressed acid tolerance genes in the ΔrstA mutant compared with EHEC O157:H7 wild type strain, Excel file S5. Differently expressed diguanylate cyclases and phosphodiesterases genes in the ΔrstA mutant compared with EHEC O157:H7 wild type strain, Excel file S6. Differently expressed Stxs and Nle genes in the ΔrstA mutant compared with EHEC O157:H7 wild type strain, Excel file S7. Differently expressed regulatory genes in the ΔrstA mutant compared with EHEC O157:H7 wild type strain.

Response regulator

Component (thermodynamics)

10.6084/m9.figshare.10184594

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Impaired Function of the Calcium-Dependent Protein Kinase, OsCPK12, Leads to Early Senescence in Rice (Oryza sativa L.)

Frontiers in Plant Science (2019)

Beifang Wang Yingxin Zhang Zhenzhen Bi Qunen Liu Tingting Xu

Premature leaf senescence affects plant yield and quality, and numerous researches about it have been conducted until now. In this study, we identified an early senescent mutant es4 in rice (Oryza sativa L.); early senescence appeared approximately at 60 dps and became increasingly senescent with the growth of es4 mutant. We detected that content of reactive oxygen species (ROS) and malonaldehyde (MDA), as well as activity of superoxide dismutase (SOD) were elevated, while chlorophyll content, soluble protein content, activity of catalase (CAT), activity of peroxidase (POD) and photosynthetic rate were reduced in the es4 mutant leaves. We mapped es4 in a 33.5Kb physical distance on chromosome 4 by map-based cloning. Sequencing analysis in target interval indicated there was an eight bases deletion mutation in OsCPK12 which encoded a calcium-dependent protein kinase. Functional complementation of OsCPK12 in es4 completely restored the normal phenotype. We used CRISPR/Cas9 for targeted disruption of OsCPK12 in ZH8015 and all the mutants exhibited the premature senescence. All the results indicated that the phenotype of es4 was caused by the mutation of OsCPK12. Overexpression of OsCPK12 in ZH8015 enhanced the net photosynthetic rate (Pn) and chlorophyll content. OsCPK12 was mainly expressed in green organs. The results of qRT-PCR analysis showed that the expression levels of some key genes involved in senescence, chlorophyll biosynthesis, and photosynthesis were significantly altered in the es4 mutant. Our results demonstrate that the mutant of OsCPK12 triggers the premature leaf senescence; however, the overexpression of OsCPK12 may delay its growth period and provide the potentially positive effect on productivity in rice.

Senescence

10.3389/fpls.2019.00052

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Mutations of flagellar genesfliC12,fliAandflhDCofEdwardsiella tardaattenuated bacterial motility, biofilm formation and virulence to fish

Journal of Applied Microbiology (2013)

Tingting Xu Ying Su Xu Ying Yang He B. Wang

The aim of this study was to investigate functions of flagellar genes fliC2, fliC12, fliA and flhDC in a bacterial fish pathogen Edwardsiella tarda.In this study, functions of flagellar genes, fliC2, fliC12 (fliC1 + fliC2), fliA and flhDC (flhD + flhC) of Edw. tarda H1 were analysed by constructing in-frame deletion mutants respectively and complementary strains fliC2(+) and fliA(+) . Electron microscopy revealed that in-frame deletion of fliC12, fliA and flhDC significantly impaired the number and length of flagellar filaments, resulting in loss of both swimming and swarming motilities of the bacteria. In addition, compared to the wild-type strain and complementary strains, the flagellum-impaired mutants exhibited reduced biofilm formation ability, showed decreased ability in adherence and internalization to Epithelioma papulosum cyprini (EPC) cells and reduced pathogenicity to zebrafish.These results indicated that fliC12, fliA and flhDC of Edw. tarda played essential roles in flagellar filaments structure, bacteria motility, biofilm formation, adherence, internalization and pathogenicity of this bacterium.This study revealed that flagella function in facilitating virulence and it may provide a new target for vaccines against Edw. tarda infection.

Marine Biology

Zhàng

Marine life

10.1111/jam.12357

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CLIP: Accelerating Features Deployment for Programmable Switch

IEEE INFOCOM 2022 - IEEE Conference on Computer Communications (2023)

Tingting Xu Xiaoliang Wang Chen Tian Yun Xiong Yun Lin

Cloud network serves a large number of tenants and a variety of applications. The continuously changing demands require a programmable data plane to achieve fast feature velocity. However, the years-long release cycle of traditional function-fixed switches can not meet this requirement. Emerging programmable switches provide the flexibility of packet processing without sacrificing hardware performance. Due to the trade-off between performance and flexibility, the current programmable switches make compromises in some aspects such as limited memory/computation resources, and lack of the capacity to realize complicated computation. The programmable switches can not satisfy the demand for network services and applications in production networks. We propose a framework that leverages host servers to extend the capability of network switches quickly, accelerates new feature deployment, and verifies new ideas in production networks. Specifically, to build the unified programmable data plane, we propose essential design and implementation challenges including a programming abstraction that allows automatically and effectively deploying network functions on switch and server clusters, allocating traffic to fully utilize the server resources, and supporting flexible scaling of the system. The quick deployment of self-defined functions in a realistic system has verified the feasibility and practicality of the proposed framework.

Forwarding plane

Network switch

Packet processing

10.1109/infocom53939.2023.10228857

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Akkermansia muciniphila identified as key strain to alleviate gut barrier injury through Wnt signaling pathway

Xin Ma Meng Li Yuanyuan Zhang Tingting Xu Xinchen Zhou

As the largest mucosal surface, the gut has built a physical, chemical, microbial and immune barrier to protect the body against pathogen invasion. The disturbance of gut microbiota aggravates pathogenic bacteria invasion and gut barrier injury. Fecal microbiota transplantation (FMT) is a promising treatment for microbiome-related disorders, where beneficial strain engraftment is a significant factor influencing FMT outcomes. The aim of this research was to explore the effect of FMT on antibiotic-induced microbiome-disordered (AIMD) model infected with enterotoxigenic Escherichia coli (ETEC). We used piglet, mouse and intestinal organoid models to explore the protective effects and mechanisms of FMT on ETEC infection. The results showed that FMT regulated gut microbiota and enhanced the protection of AIMD piglets against ETEC K88 challenge, as demonstrated by reduced intestinal pathogen colonization and alleviated gut barrier injury. Akkermansia muciniphila ( A. muciniphila ) and Bacteroides fragilis ( B. fragilis ) were identified as two strains that may play key roles in FMT. We further investigated the alleviatory effects of these two strains on ETEC infection in AIMD mice model, which revealed that A. muciniphila and B. fragilis relieved ETEC-induced intestinal inflammation by maintaining the proportion of Treg/Th17 cells and epithelial damage by moderately activating the Wnt/β-catenin signaling pathway, while the effect of A. muciniphila was better than B. fragilis . We therefore identified whether A. muciniphila protected against ETEC infection using basal-out and apical-out intestinal organoid models. A. muciniphila did protect the intestinal stem cells and stimulate proliferation and differentiation of intestinal epithelium, and the protective effects of A. muciniphila was reversed by Wnt inhibitor. FMT alleviated ETEC-induced gut barrier injury and intestinal inflammation in AIMD model. A. muciniph ila was identified as key strain in FMT to promote proliferation and differentiation of intestinal stem cells by mediating the Wnt/β-catenin signaling pathway.

Akkermansia muciniphila

Strain (injury)

10.7554/elife.92906.4

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Akkermansia muciniphila identified as key strain to alleviate gut barrier injury through Wnt signaling pathway

Xin Ma Meng Li Yuanyuan Zhang Tingting Xu Xinchen Zhou

Akkermansia muciniphila

Strain (injury)

10.7554/elife.92906.3

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Novel plasmid-mediated CMY variant (CMY-192) conferring ceftazidime-avibactam resistance in multidrug-resistant Escherichia coli

Antimicrobial Agents and Chemotherapy (2024)

Tingting Xu Weiyuan Wu Lili Huang Bin Liu Q. Y. Zhang

ABSTRACT The rapid rise of multidrug resistance (MDR) among Gram-negative bacteria has accelerated the development of novel therapies. Ceftazidime-avibactam (CZA) is a novel β-lactam/β-lactamase inhibitor recently approved for the treatment of limited infectious diseases. Here, we describe a novel CMY variant, CMY-192, that confers high-level resistance to CZA. This gene was detected in a clinical MDR Escherichia coli strain (Ec73552) isolated from an outpatient with a community-acquired urinary tract infection who had not received prior CZA treatment. Ec73552 was typed as O101:H9-ST10, a high-risk clone associated with human and animal diseases. Ec73552 was able to colonize the bladder in a mouse model, suggesting that this strain was uropathogenic. CMY-192 shared the highest amino acid identity (98.95%) with CMY-172 and conferred at least a 32-fold increase in CZA MIC (from ≤0.125/4 to 8/4 mg/L) when cloned into a CZA-susceptible E. coli DH5α strain. Knockout of CMY-192 in Ec73552 resulted in a 256-fold reduction in CZA MIC (from 64/4 to 0.25/4 mg/L). CMY-192 was encoded on an IncB/O/K/Z-type plasmid (pCMY192). Conjugation assays confirmed that pCMY192 was self-transmissible, resulting in a 256-fold increase in the CZA MIC of the recipient. Notably, pCMY192 cured in Ec73552 did not confer a growth advantage, while the conjugant exhibited reduced biomass and growth rate, indicating that fitness costs imposed by pCMY192 may have been compensated in Ec73552. Our findings highlight the importance of continuous monitoring of CZA susceptibility to prevent the spread of resistance in clinical settings.

Ceftazidime/avibactam

10.1128/aac.00906-24

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Epidemiology and Mechanisms of Ceftazidime–Avibactam Resistance in Gram-Negative Bacteria

Engineering (2021)

Tingting Xu Yuqi Guo Yang Ji Baohong Wang Kai Zhou

Carbapenem resistance presents a major challenge for the global public health network, as clinical infections caused by carbapenem-resistant organisms (CRO) are frequently associated with significant morbidity and mortality. Ceftazidime–avibactam (CAZ–AVI) is a novel cephalosporin/β-lactamase inhibitor combination offering an important advance in the treatment of CRO infections. CAZ–AVI has been reported to inhibit the activities of Ambler classes A, C, and some class D enzymes. However, bacterial resistance has been emerging shortly after the introduction of this combination in clinical use, with an increasing trend. Understanding these resistance mechanisms is crucial for guiding the development of novel treatments and aiding in the prediction of underlying resistance mechanisms. This review aims to systematically summarize the epidemiology of CAZ–AVI-resistant strains and recently identified resistance mechanisms of CAZ–AVI, with a focus on the production of β-lactamase variants, the hyperexpression of β-lactamases, reduced permeability, and overexpressed efflux pumps. The various mechanisms of CAZ–AVI resistance that have emerged within a short timescale emphasize the need to optimize the use of current agents, as well as the necessity for the surveillance of CAZ–AVI-resistant pathogens.

Ceftazidime/avibactam

Efflux

Avibactam

10.1016/j.eng.2020.11.004

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Determination of the Infectious Agent of Translucent Post-Larva Disease (TPD) in Penaeus vannamei

Pathogens (2020)

Ying Zou Guosi Xie Tianchang Jia Tingting Xu Chong Wang

A new emerging disease called "translucent post-larvae disease" (TPD) or "glass post-larvae disease" (GPD) of Penaeus vannamei, characterized by pale or colorless hepatopancreas and digestive tract, has become an urgent threat to the shrimp farming industry. Following this clue that treatment of an antibacterial agent could alleviate the disease, systematic investigation of the potential infectious agent of TPD was conducted using bacterial identification and artificial challenge tests to fulfill Koch's postulates. A dominant bacterial isolate, Vp-JS20200428004-2, from the moribund individuals was isolated and identified as Vibrio parahaemolyticus based on multi-locus sequence analysis. However, Vp-JS20200428004-2 differed from the V. parahaemolyticus that caused typical acute hepatopancreatic necrosis disease. Immersion challenge tests revealed that Vp-JS20200428004-2 could cause 100% mortality within 40 h at a dose of 1.83 × 106 CFU/mL, and experimental infected shrimp showed similar clinical signs of TPD. The Vp-JS20200428004-2 could be re-isolated and identified from the experimental infected individuals. Moreover, histopathological analysis of diseased samples indicated that Vp-JS20200428004-2 caused severe necrosis and sloughing of epithelial cells of the hepatopancreas and midgut in shrimp individuals both naturally and experimentally infected. Our present results indicated that Vp-JS20200428004-2 is a highly virulent infectious agent associated with the TPD and deserves further attention.

Hepatopancreas

Penaeus

Litopenaeus

Bacterial disease

10.3390/pathogens9090741

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Citations (27)