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Transcriptomic Response to Yersinia pestis:RIG-I Like Receptor Signaling Response Is Detrimental to the Host against Plague 被引量:2
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作者 Zongmin Du Huiying yang +12 位作者 Yafang Tan Guang Tian Qingwen Zhang Yujun Cui yanfeng yan Xiaohong Wu Zuyun Chen Shiyang Cao Yujing Bi yanping Han Xiaoyi Wang Yajun Song Ruifu yan 《Journal of Genetics and Genomics》 SCIE CAS CSCD 2014年第7期379-396,共18页
Bacterial pathogens have evolved various mechanisms to modulate host immune responses for successful infection. In this study, RNA- sequencing technology was used to analyze the responses of human monocytes THP1 to Ye... Bacterial pathogens have evolved various mechanisms to modulate host immune responses for successful infection. In this study, RNA- sequencing technology was used to analyze the responses of human monocytes THP1 to Yersinia pestis infection. Over 6000 genes were differentially expressed over the 12 h infection. Kinetic responses of pathogen recognition receptor signaling pathways, apoptosis, antigen processing, and presentation pathway and coagulation system were analyzed in detail. Among them, RIG-I-like receptor (RLR) signaling pathway, which was established for antiviral defense, was significantly affected. Mice lacking MAVS, the adaptor of the RLR signaling pathway, were less sensitive to infection and exhibited lower IFN-13 production, higher Thl-type cytokines IFN-γ and IL-12 production, and lower Th2-type cytokines IL-4 and IL-13 production in the serum compared with wild-type mice. Moreover, infection of pathogenic bacteria other than E pestis also altered the expression of the RLR pathway, suggesting that the response of RLR pathway to bacterial infection is a universal mechanism. 展开更多
关键词 Yersinia pestis Innate immunity RIG-I-like receptor signaling RNA-seq Transcriptomic response
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IL-17A-dependent gut microbiota is essential for regulating diet-induced disorders in mice 被引量:7
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作者 Yujing Bi Chunxiao Li +16 位作者 Lin Liu Jiyuan Zhou Zhengchao Li Huimin Deng Chunyan Wu yanping Han Yajun Song Yafang Tan Xiaoyi Wang Zongmin Du Yujun Cui yanfeng yan Fachao Zhi Guangwei Liu Nan Qin Heping Zhang Ruifu yang 《Science Bulletin》 SCIE EI CAS CSCD 2017年第15期1052-1063,共12页
The gut microbiota plays a key role in obesity and related metabolic disorders, and multiple factors including diet, host genotype, and age regulate it. Many studies have examined the contribution of extrinsic factors... The gut microbiota plays a key role in obesity and related metabolic disorders, and multiple factors including diet, host genotype, and age regulate it. Many studies have examined the contribution of extrinsic factors to the regulation of the gut microbiota, but the importance of the host genetic constitution cannot be ignored, lnterleukin 17A (lL-17A), a pro-inflammatory cytokine, is important in the defense against infection and diseases. Here, we investigated the association among IL-17, a high-fat diet (HFD), and the gut microbiota. Mice deficient in 1L-17A were resistant to diet-induced obesity and related diseases. Compared with the I1-17a^-/1 mice, wild-type (WT) mice challenged with HFD showed obvious weight fluctuations, such as those seen in type 2 diabetes, and hematological changes similar to those associated with metabolic syndrome. However, housing WT mice and Il-17a^-/- mice together signifi- cantly alleviated these symptoms in the WT mice. A metagenomic analysis of the mouse feces indicated that the microbial community compositions of these two groups differed before HFD feeding. The HFD mediated shifts in the gut microbial compositions, which were associated with the mouse phenotypes. We also identified potentially beneficial and harmful species present during this period, and drew net- works of the most abundant species. A functional analysis indicated pathway changes in the WT and I1-17a^- /- mice when fed the HFD. Collectively, these data underscore the importance of the host factor IL-17A in shaping and regulating the gut microbiota, which conversely, influences the host health. 展开更多
关键词 Gut microbiota Obesity IL-17A Metagenomics
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The Establishment and Application of Mobile Electronic Surveillance System for Infectious Diseases with the Help of China—Sierra Leone,2016-Present 被引量:1
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作者 Guangyu Zhao Haorong Chen +13 位作者 yanfeng yan Jiafu Jiang Lei Lin Baogui Jiang Foday Sahr Stephen Sevalie Qiang Xu Jinjin Chen Henry Saidu Bangura Kandeh Bassie Kargbo Yajun Song Wei Liu Liqun Fang yansong Sun 《China CDC weekly》 2021年第36期763-768,共6页
Introduction:Infectious disease surveillance has long been a challenge for low-income countries like Sierra Leone.Traditional approaches based on paper and Short Message Service(SMS)were subject to severe delays in ob... Introduction:Infectious disease surveillance has long been a challenge for low-income countries like Sierra Leone.Traditional approaches based on paper and Short Message Service(SMS)were subject to severe delays in obtaining,transmitting,and analyzing information.Methods:During the China aid operation for fighting Ebola since the end of 2014,a mobile electronic surveillance system for infectious diseases(MESSID)was developed in collaboration with the Republic of Sierra Leone Armed Forces(RSLAF),which comprised an Android-based reporting system and a complementary web-based program designed by Active Server Page.NET(ASP.NET)with the main functions including surveillance,real-time reporting,and risk assessment of infectious diseases.Results:MESSID was successfully registered in June 2016 and had been used by all medical and health institutions in RSLAF.From June 1,2016 to July 5,2021,34,419 cases were diagnosed with 47 infectious diseases of 5 categories,with a total of 42 clinical symptoms.Compared to traditional approaches based on paper and SMS,the MESSID showed flexibility,high efficiency,convenience,and acceptability.Discussion:MESSID is an accessible tool for surveillance of infectious diseases in Sierra Leone and possibly in other African countries with similar needs,capable of improving timeliness of disease reporting,thus rendering a timely outbreak detection and response. 展开更多
关键词 RENDERING SERVER Sierra
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