| 1 | Pseudomonas aeruginosa:pathogenesis,virulence factors,antibiotic resistance,interaction with host,technology advances and emerging therapeutics显示文摘Pseudomonas aeruginosa(P.aeruginosa)is a Gram-negative opportunistic pathogen that infects patients with cystic fibrosis,burn wounds,immunodeficiency,chronic obstructive pulmonary disorder(COPD),cancer,and severe infection requiring ventilation,such as COVID-19.P.aeruginosa is also a widely-used model bacterium for all biological areas.In addition to continued,intense efforts in understanding bacterial pathogenesis of P.aeruginosa including virulence factors(LPS,quorum sensing,two-component systems,6 type secretion systems,outer membrane vesicles(OMVs),CRISPR-Cas and their regulation),rapid progress has been made in further studying host-pathogen interaction,particularly host immune networks involving autophagy,inflammasome,noncoding RNAs,cGAS,etc.Furthermore,numerous technologic advances,such as bioinformatics,metabolomics,scRNA-seq,nanoparticles,drug screening,and phage therapy,have been used to improve our understanding of P.aeruginosa pathogenesis and host defense.Nevertheless,much remains to be uncovered about interactions between P.aeruginosa and host immune responses,including mechanisms of drug resistance by known or unannotated bacterial virulence factors as well as mammalian cell signaling pathways.The widespread use of antibiotics and the slow development of effective antimicrobials present daunting challenges and necessitate new theoretical and practical platforms to screen and develop mechanism-tested novel drugs to treat intractable infections,especially those caused by multi-drug resistance strains.Benefited from has advancing in research tools and technology,dissecting this pathogen’s feature has entered into molecular and mechanistic details as well as dynamic and holistic views.Herein,we comprehensively review the progress and discuss the current status of P.aeruginosa biophysical traits,behaviors,virulence factors,invasive regulators,and host defense patterns against its infection,which point out new directions for future investigation and add to the design of novel and/or alternative therapeutics to combat this clinically significant pathogen. | Shugang Qin Wen Xiao Chuanmin Zhou Qinqin Pu Xin Deng Lefu Lan Haihua Liang Xiangrong Song Min Wu | 2022 | Signal Transduction and Targeted Therapy2022，7，7： | 5 |
| 2 | Lyn prevents aberrant inflammatory responses to Pseudomonas infection in mammalian systems by repressing a SHIP-1-associated signaling cluster显示文摘The pleiotropic Src kinase Lyn has critical roles in host defense in alveolar macrophages against bacterial infection,but the underlying mechanism for Lyn-mediated inflammatory response remains largely elusive.Using mouse Pseudomonas aeruginosa infection models,we observed that Lyn^(−/−)mice manifest severe lung injury and enhanced inflammatory responses,compared with wild-type littermates.We demonstrate that Lyn exerts this immune function through interaction with IL-6 receptor and cytoskeletal protein Ezrin via its SH2 and SH3 domains.Depletion of Lyn results in excessive STAT3 activation,and enhanced the Src homology 2-containing inositol-5-phopsphatase 1(SHIP-1)expression.Deletion of SHIP-1 in Lyn^(−/−)mice(double knockout)promotes mouse survival and reduces inflammatory responses during P.aeruginosa infection,revealing the rescue of the deadly infectious phenotype in Lyn deficiency.Mechanistically,loss of SHIP-1 reduces NF-κB-dependent cytokine production and dampens MAP kinase activation through a TLR4-independent PI3K/Akt pathway.These findings reveal Lyn as a regulator for host immune response against P.aeruginosa infection through SHIP-1 and IL-6/STAT3 signaling pathway in alveolar macrophages. | Rongpeng Li Lizhu Fang Qinqin Pu Ping Lin Austin Hoggarth Huang Huang Xuefeng Li Guoping Li Min Wu | 2016 | Signal Transduction and Targeted Therapy2016，1，1： | 1 |
| 3 | 鲍曼不动杆菌CRISPR相关蛋白Csy1对耐药性和毒力的影响显示文摘采用RecAb同源重组系统,将携带I-Fb亚型CRISPR-Cas系统的鲍曼不动杆菌临床分离株AB43的csy1基因敲除,观察野生株(AB43)和缺失株(AB43Δcsy1)的耐药性、生物膜形成以及小鼠致死率等生物学性状变化,并通过转录组测序分析两者间的差异表达基因。与野生株相比,csy1的缺失显著提高突变株的耐药水平和体外形成生物膜的能力,且AB43Δcsy1感染组小鼠的存活率与AB43感染组相比显著降低,提示其毒力有所提高。RNA-seq分析结果显示,csy1的缺失能影响细菌与抗生素耐药性、毒力以及代谢相关基因的表达,推测是引起AB43Δcsy1表型变化的主要原因。结果提示Csy1蛋白可通过调节自身基因表达抑制鲍曼不动杆菌的耐药性、生物膜形成及致病性。这说明创造有利于维持CRISPR-Cas系统的环境,保证CRISPR-Cas系统阳性菌株处于进化优势地位,使鲍曼不动杆菌保持低毒力和抗生素敏感状态。 | 李梦影 孙晓利 王宇航 杨洁 郑文浩 何香玲 季诗雨 焦红梅 郭停停 李国才 | 2021 | 扬州大学学报(农业与生命科学版)2021，42，1： | 0 |
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